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1
Panganiban, April Rose. "Task load and evaluative stress in a multiple UAV control simulation: The protective effect of executive functioning ability." University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1378215257.
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Maglara, Antonia. "An investigation of the role of oxidative stress and the potential protective effect glutamine supplementation in an animal model of systematic inflammation." Thesis, University of Liverpool, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269718.
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Kojima, Hiroshi. "Granulocyte colony-stimulating factor attenuates oxidative stress-induced apoptosis in vascular endothelial cells and exhibits functional and morphological protective effect in oxygen-induced retinopathy." Kyoto University, 2011. http://hdl.handle.net/2433/142077.
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Phang, Ing Chia. "Response of Arabidopsis thaliana seedlings to lead exposure." Thesis, University of Canterbury. School of Biological Sciences, 2010. http://hdl.handle.net/10092/4467.
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Lead (Pb) is one of the most commonly occurring, highly persistent and widely distributed heavy metal contaminants in the environment. It has a tendency to bioaccumulate in animals and plants, and potentially, it is able to enter the human food chain where it poses a hazard to public health. Generally, conventional remediation technologies applied to decontaminate heavy metals from groundwater and soils are very costly. Hence, phytoremediation has emerged as an ecologically friendly and economically attractive technology that uses green plants to clean up heavy metal contaminated sites. However, a lack of knowledge of the biological processes associated with plant responses to Pb (e.g. Pb uptake, accumulation, translocation, and tolerance) has been a bottleneck for the application of Pb phytoremediation in the field. A model genetic system of higher plants, Arabidopsis thaliana, was selected to further examine the physiological, biochemical and molecular events occuring in plants under Pb stress.
The overall aim of this project was to obtain a better understanding of plant responses to Pb contaminants in the early developmental stages of A. thaliana seedlings. This research encompassed the physiological responses of A. thaliana seedlings to Pb exposure, monitoring their antioxidative defence systems, and investigating the participation of annexin 1 in the response to Pb-mediated oxidative stress. This research also assessed the protective effect of nitric oxide on Pb-induced toxicity of A. thaliana seedlings and it isolated a putative Pb tolerant mutant from an EMS-mutagenized M2 population. A multiexperimental approach was adopted to achieve these objectives.
A. thaliana seedlings were grown on modified Huang & Cunningham (1996) nutrient solution containing 0.8% (w/v) agar, with and without Pb(NO3)2, under controlled conditions. A. thaliana seedlings were insensitive to Pb during seed germination. In treatments with up to 200 μM Pb(NO₃)₂, morphological changes and inhibition of root growth were observed in the 7-d-old seedlings. A tolerance index revealed that Pb(NO₃)₂ concentration of 75 μM and higher brought about more than 50% root growth inhibition. Pb was predominantly retained in the roots. Analysis using a graphite furnace atomic absorption spectroscopy indicated that the level of Pb accumulation in A. thaliana roots was greatly dependent on the Pb(NO₃)₂ concentrations, but only a small fraction of the accumulated Pb was translocated to the shoots (18 - 43%). Transmission electron microscopy analysis showed that Pb was mainly immobilized in the cell walls and intercellular spaces. This was interpreted as a mechanism that minimizes the entry of Pb into cells and interference with cellular functions. Pb that gained entry into the cytoplasm was sequestered into the vacuoles.
The toxicity of Pb in the cytosol of A. thaliana seedlings was studied by measuring the H₂O₂ and lipid hydroperoxide levels using a microplate reader. When the Pb(NO₃)₂ concentration in the growth medium was 100 μM, the 7-d-old seedlings contained 2.2-fold higher H₂O₂ and 9.6-fold higher lipid hydroperoxide than the control without Pb(NO₃)₂. This was followed by an up-regulation of the activity of antioxidative enzymes, including superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPX), and general peroxidase (POD) by 2.1-, 3.2-, 2.3-, 1.8- and 4.6-fold, respectively, compared with the control. Pb toxicity is known to trigger oxidative stress, but A. thaliana seedlings appeared to be capable of activating cell rescue, defending themselves against harmful oxidative stress and also acclimating to Pb. Data from physiological and biochemical analysis indicate that a combination of avoidance and tolerance mechanisms exists in Pb-treated A. thaliana seedlings to maintain the essential cellular metabolism for survival.
Real-time reverse-transcription polymerase chain reaction was used to show the involvement of AnnAt1 in the response of 7-d-old A. thaliana seedlings to a high threshold concentration of Pb. When the seedlings were treated with 100 μM Pb(NO₃)₂, AnnAt1 message levels were up-regulated by 2.12-fold. Pb-mediated oxidative stress may be a component of AnnAt1 gene expression. AnnAt1 potentially could be invoked to reduce the toxic effects of Pb stress by acting as ROS and/or Ca²⁺ signals, as a membrane protector, in detoxification of excessive ROS, or in sequestration of Pb.
Pb stress symptoms were less evident in seedlings pre-treated with 1 mM sodium nitroprusside (SNP), a nitric oxide (NO) donor. The present study found that exogenous NO did not alter Pb transport into the plants or efflux pumping of Pb at the plasma membrane. However, NO conferred protection to 7-d-old A. thaliana seedlings primarily by acting as an antioxidant or a signal for actions to scavenge excessive ROS level. The application of exogenous NO before subjecting to 100 μM Pb(NO₃)₂ decreased H₂O₂ back to its original level, and reduced 50% lipid hydroperoxide in the Pb-treated seedlings. As a result, the antioxidative enzyme activities in Pb-exposed seedlings pre-treated with SNP were 23 - 45% lower than those without SNP pre-treatment. Less antioxidative enzyme activities were probably needed to counteract the reduced amount of Pb-induced ROS in A. thaliana seedlings.
A post-germination procedure involving prolonged exposure to 150 μM Pb(NO₃)₂ was developed to screen an EMS-mutagenized M2 population of A. thaliana. Potential Pb tolerant mutants were selected based on the ability to grow with their roots penetrating into the medium and maintain purple-green leaves without wilting. A minority of the survivors appeared to go into a resting stage and they seemed to have altered transporters that prevented Pb from entering the cells. Only one putative Pb mutant (M3-1) was recovered from the rescue and set seeds. The M₄ generation of this putative Pb mutant was re-screened for phenotypic confirmation and to determine the regulation of AnnAt1. The 7-d-old putative Pb mutant seemed to display enhanced root and shoot growth in the presence of 150 μM Pb(NO₃)₂ compared to the wild-type seedlings. The transcript level of AnnAt1 in this putative Pb tolerant mutant increased by 2.19-fold when exposed to 150 μM Pb(NO₃)₂.
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Nazari, Qand Agha. "Protective effects of luteolin and curcumin on oxidative stress induced by sodium nitroprusside in the brain." 京都大学 (Kyoto University), 2013. http://hdl.handle.net/2433/175235.
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Subramaniam, Sudhakar Raja. "Protective effects of dietary coumarins on disease conditions associated with oxidative stress : neurodegenerative diseases and cancer." Thesis, University of Strathclyde, 2010. http://oleg.lib.strath.ac.uk:80/R/?func=dbin-jump-full&object_id=14444.
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Boyle, Neil Bernard. "Measuring the effects of stress on cognitive function in real-world and laboratory contexts : the potential protective effects of phospholipid supplementation." Thesis, University of Leeds, 2013. http://etheses.whiterose.ac.uk/6398/.
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There is a well-defined relationship between stress and cognition. The intake of phospholipids has the potential to attenuate responses to stress and thus protect cognitive performance. The aims of this thesis were (a) develop suitable methodologies, both in the real-world and laboratory, to examine the effects of stress on cognition; (b) identify characteristics of individuals who may be particularly stress vulnerable; and (c) assess the potential for a phospholipid intervention to attenuate the response to stress and the impact of this stress exposure on cognitive function. These aims were addressed in four studies. Studies 1 – 3 aimed to identify a number of design and methodological conditions suitable for a phospholipid intervention assessing cognitive performance under stress (Study 4). The identification of a naturalistic or laboratory stress context capable of eliciting cortisol responses over repeated exposures, selection of cognitive tests sensitive to stress impairment, and characterising individuals with an increased tendency towards high cortisol responsivity to stress were the key preparatory methodological factors examined in Studies 1 – 3. Studies 1 (N = 16) and 2 (N = 17) explored the feasibility of employing a real-world audition stress context for a dietary intervention. Whilst this context was sufficient to elicit significant cortisol responses (Study 1), this was not consistently shown (Study 2), and suggestive of poor test-retest reliability. Study 3 (N = 24) demonstrated that a combined physical/psychosocial laboratory stressor was sufficient to elicit significant, and comparable, cortisol responses over repeated exposures. Three tests of prefrontal cortex-mediated cognitive function (n-back, ospan, and task-switch test) were demonstrated to be sensitive to stress impairment (Studies 2 – 3) and the Perfectionism: Organisation dimension of perfectionism emerged as a positive predictor of cortisol responsivity (Studies 1 – 3). The laboratory stressor, identified cognitive tests, and a sample selected on the basis of high perfectionist tendency, were identified as appropriate methodologies for the dietary intervention. These methodologies were employed in a randomised placebo-controlled six week phospholipid intervention (N = 54) assessing cognitive performance after an acute physical/psychosocial stressor (pre- and post-intervention). Phospholipid intake was associated with increased cortisol response, and significant elevations in sympathetic and subjective arousal. Cognitive performance was unaffected by phospholipid intake. A trend for attenuated anticipatory subjective stress suggested a modest stress-buffering effect of phospholipids. Further examination of the relationship between perfectionism and cortisol, and determinants of reduced habituation to the laboratory stressor employed, are warranted. The methodological advances developed herein offer a suitable framework for future research further assessing the potential stress-buffering effect of phospholipids in samples characterised by cognitive vulnerabilities (e.g., the elderly).
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Acioli, PorfÃrio Cezar Passos. "Protective effects of acupuncture and electroacupuncture on oxidative stress and inflammation due to testis torsion/detorsion in rats." Universidade Federal do CearÃ, 2014. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=12207.
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The efects of acupuncture (Ac) and Electroacupuncture (EAc) were evaluated using
an experimental rat model of ischemia/reperfusion (IR) of the testis. In Traditonal
Chinese Medicine, these forms of therapies are used in the promotion of organic
equilbrium, through stimulation of specifc neurotransmiters producing nerve
pathways, resulting in a analgesic and anti-nflammatory autonomic regulatory.
response. In the study, 30 male Wistar rats, 279.6g average weight (230-30 g) were
randomly divided into five groups. Al rats received intraperitoneal anesthesia
(Ketamine 10 90mgKgXilazina mgKg), at the begining of the experiment, before the
detorsion and at the end of the experiment. G1 group was submited to torsion of the
testicle (TT), two complete turns (720Â) with immediate detorsion (sham). The other
groups (G2IR, G3Ac, G4EAc2 and G5EAc10) were submited to TT during 3 hours,
folowed by detorsion and reperfusion during 4 hours. Five minutes before the
detorsion Ac (G3Ac) or EAc (G4EAc2, G5EAc10) was aplied, under anesthesia, for
5 minutes. Next the testis was detorsioned and reperfused for 4 hours. At the end
blod samples the right testicle were colected. Evaluated parameters included
determination of reduced Glutathione (GSH), Malonaldehyde (MDA),
Myeloperoxidase (MPO) and histopathology of the testicle. EAc (2 and 10 Hz)
promoted signifcant increase in concentrations of GSH in plasma and in the rat estis
of G4-G5, compared to the control G1. Ac did not alter signifcantly the concentrations
of GSH in the G3 group compared to the G1. There was signifcant increase of MDA
in tisue in groups G4-G5 and plasma MDA in al groups, compared to the G1. EAc (2
Hz and 10 Hz) signifcantly decreased the activity of MPO in the testis of rats
subjected to TT (G4-G5), compared to the control G1. No signifcant diferences were
observed in the activity of MPO comparing groups G4-G5 to group G1. It is concluded
that EAc stimulation (2 and 10 Hz) atenuates oxidative stres and inflammatory
response in rats subjected to testicular torsion/detorsion.<br>Os efeitos da Acupuntura (Ac) e da Eletroacupuntura (EAc) foram avaliados
utilzando um modelo experimental de isquemia/reperfusÃo (I/R) do testÃculo em rato. Na Medicina Tradicional Chinesa, esas formas de terapias sÃo utilzadas na
promoÃÃo do equilÃbrio orgÃnico, mediante estÃmulo de vias nervosas produtoras de
neurotransmisores especÃficos, resultando em uma resposta anti-nflamatÃria,
analgÃsica e reguladora autonÃmica. No experimento, 30 ratos Wistar machos, peso
mÃdio 279,6 g (230-30g) foram distribuÃdos aleatoriamente em cinco grupos. Todos
os ratos receberam anestesia intraperitonial (Cetamina 90mg/Kg+Xilazina 10 mg/Kg),
no inicio do experimento, antes da destorÃÃo e ao tÃrmino do experimento. O grupo
G1 foi submetido à torÃÃo do testÃculo (TT), duas voltas completas (720Â) com
imediata destorÃÃo (sham). Os demais grupos (G2IR, G3Ac, G4EAc2 e G5EAc10)
foram submetidos à TT durante 3 horas, seguido de destorÃÃo e reperfusÃo durante
4 horas. Cinco minutos antes da destorÃÃo procedeu-se à aplicaÃÃo da Ac (G3Ac) ou
EAc (G4EAc2, G5EAc10), sob anestesia por 5 minutos. Findo ese tempo realizou- se à destorÃÃo do testÃculo e permitu-se a reperfusÃo por 4 horas. Ao tÃrmino foram
coletadas amostras de sangue arterial e de tecido (testÃculo direito). ParÃmetros
avaliados incluÃram determinaÃÃo de Glutationa (GSH) reduzida, MalonaldeÃdo
(MDA), Mieloperoxidase (MPO) e histopatologia do testÃculo. A EAc (2 e 10Hz)
promoveu aumento signifcante nas concentraÃÃes de GSH no plasma e no testÃculo
dos ratos dos grupos G4-G5, comparados ao controle G1. A Ac nÃo alterou
signifcativamente as concentraÃÃes de GSH no grupo G3 comparado ao G1. Houve
aumento signif cante do MDA tecidual nos grupos G4-G5 e do MDA plasmÃtico em
todos os grupos, comparados ao G1. A EAc (2Hz e 10Hz) diminuiu signifcativamente
a atividade da MPO no testÃculo dos ratos submetidos à torÃÃo do testÃculo (grupos
G4-G5), comparados ao controle G1. NÃo foram observadas diferenÃas signifcantes
na atividade da MPO comparando-se os grupos G4-G5 ao grupo G1. Conclui-se que
a aplicaÃÃo de EAc de 2/10Hz promove proteÃÃo local e sistÃmica sobre o estrese
oxidativo e diminuiÃÃo da resposta inflamatÃria em ratos sadios submetidos a
torÃÃo/destorÃÃo do testÃculo.
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VanGilder, Reyna. "Examining the protective effects of sesamol on oxidative stress associated blood-brain barrier dysfunction in streptozotocin-induced diabetic rats." Morgantown, W. Va. : [West Virginia University Libraries], 2009. http://hdl.handle.net/10450/10541.
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Thesis (Ph. D.)--West Virginia University, 2009.<br>Title from document title page. Document formatted into pages; contains xi, 165 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 131-163).
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Konstantinidou, Valentini. "Molecular mechanisms involved in the protective effect of Mediterranean diet and olive oil consumption in humans." Doctoral thesis, Universitat Pompeu Fabra, 2010. http://hdl.handle.net/10803/7208.
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The scope of the present work was to investigate whether the protective role of the traditional Mediterranean diet (TMD), and virgin olive oil (VOO) rich in phenolic compounds (PC), towards cardiovascular disease can be mediated through gene expression changes. Two trials were performed to assess the in vivo nutrigenomic effects of TMD and VOO in healthy volunteers. The results point out: a) significant gene expression changes of those genes related with cardiovascular-risk processes after VOO ingestion; b) a down-regulation in the expression of atherosclerosis-related genes after a 3-month intervention with a TMD; and c) an olive oil PC health-protective nutrigenomic effect within the frame of the TMD. Changes in gene expression were concomitant with decreases in oxidative damage and systemic inflammation markers. Data from our studies provide further evidence to recommend both the TMD and the VOO as a useful tool for the prevention of atherosclerosis.<br>El objetivo de este estudio es investigar si el papel protector de la dieta Mediterránea tradicional (TMD) y del aceite de oliva virgen (VOO), rico en compuestos fenólicos (PC), puede ser mediado a través de cambios en la expresión génica. Se realizaron dos ensayos clínicos para evaluar los efectos nutrigenómicos de la TMD y del VOO, in vivo, en voluntarios sanos. Los resultados mostraron a) cambios en la expresión génica de genes relacionados con el riesgo cardiovascular tras la ingestión del aceite virgen de oliva, b) una infra-expresión en la expresión de genes relacionados con el proceso aterosclerótico tras una intervención con TMD de 3 meses y c) que los compuestos fenólicos del aceite de oliva ejercen un efecto nutrigenómico protector en el marco de la TMD. Los cambios en la expresión génica fueron coherentes.
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Davis, Lauren Zagorski. "Characteristics of life stress experienced prior to the diagnosis of ovarian cancer: Differential effects on psychosocial functioning and the role of protective resources." Diss., University of Iowa, 2017. https://ir.uiowa.edu/etd/5744.
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Little research has examined the effect of non-cancer life stressors on psychological well-being and recurrence in patients with cancer, and results have been mixed. Furthermore, no studies have examined specific types of stress, including loss, danger, and entrapment in patients with cancer, utilizing data obtained from the Life Events and Difficulties Schedule. Given that specifics stressors have been associated with certain psychological responses, this study sought to obtain a more nuanced understanding of the relationship between life stress and psychological well-being. This was examined in a sample of 135 women with ovarian cancer prior to surgery and during the year after diagnosis using latent growth curve analyses. Models of protective psychosocial resources examining social support, mastery, self-acceptance, and purpose in life as potential moderators and mediators of the relationship between life stress and psychosocial outcomes were also evaluated.
Results indicated that cancer-related losses were most closely associated with psychological well-being across several analyses, and non-cancer losses had the greatest impact on psychological outcomes when cancer-related loss was low. Non-cancer losses were significantly related to greater fatigue prior to surgery. Additionally, major non-cancer danger stressors were associated with greater distress prior to surgery. In this sample, no stressors were significantly related to cancer recurrence. Social support was the most consistent moderator of life stress on psychological well-being, and its effects on distress and depression at baseline were mediated through self-acceptance. These findings highlight the importance of both cancer- and non-cancer-related stressors on psychological wellbeing among cancer patients in their first year following surgery and furthers our understanding of the role of protective psychosocial factors. This study has significant implications for distress screenings in patients with cancer, psychological interventions, and future research.
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SILVA, Luís Cláudio Nascimento da. "Avaliação da expressão de citocinas, óxido nítrico e de Receptores toll like em macrófagos peritoneais tratados in vitro com a lectina nativa e recombinante de sementes de Cratylia mollis." Universidade Federal de Pernambuco, 2013. https://repositorio.ufpe.br/handle/123456789/16321.
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Previous issue date: 2013-09-09<br>FACEPE<br>As lectinas são proteínas conhecidas por sua capacidade de ligar específica e reversivelmente a carboidratos resultando em uma variedade de propriedades biológicas. Este trabalho tem por objetivo avaliar os efeitos imunomodulador e citoprotetor das lectinas Cramoll 1,4 (pCramoll) e rCramoll 1 (rCramoll). Na determinação da ação imunomoduladora macrófagos peritoneais de camundongos Balb/c foram tratados com diferentes concentrações das lectinas (0,625-10 μM) e foram analisados os efeitos na produção óxido nítrico (NO), viabilidade celular, produção de ânion superóxido, alterações no potencial de membrana mitocondrial (ΔΨm) e na fagocitose de Staphylococcus aureus. A produção de citocinas pró-inflamatorias (IL-1β, IL-6, INF-γ e TNF-α) foi avaliada em macrófagos infectados e não infectados com S. aureus. Ambas lectinas induziram significantemente a produção de NO e de citocinas. As proteínas foram consideradas não-citotóxicas pelo ensaio com MTT, entretanto a análise por Citometria de Fluxo revelaram um aumento de células mortas. A produção de superóxido foi estimulada pelas lectinas o que foi confirmado pelas mudanças induzidas no ΔΨm. A ação fagocítica dos macrófagos foi aumentada em 27,1% e 22,47% após o tratamento destes com pCramoll e rCramoll . Por fim, as lectinas inibiram a expressão de TNF-α e IL-6 e estimularam a produção de IL-1β e INF-γ por macrófagos infectados por S. aureus. Paralelamente, o potencial protetor das lectinas contra a morte celular induzida pelo estresse oxidativo foi avaliada. Para tanto, células Vero (fibroblastos renais de macaco) foram pré-tratadas com crescentes concentrações das lectinas (0,625-10 μM) por 30 minutos e em seguida foram expostas ao H2O2 (1 mM). Após 24 horas, o efeito citoprotetor foi avaliado. Os mecanismos celulares envolvidos foram determinados por citometria de fluxo envolvendo: proteção contra morte celular, danos nos lisossomos e DNA, produção de ânion superóxido (MitoSOX), alterações no potencial de
membrana mitocondrial (ΔΨm) e proliferação celular. pCramoll e rCramoll atenuaram a citotoxicidade induzida por H2O2 de forma dose-dependente, os efeitos máximos foram 96.85 ± 15.59% (rCramoll) e 59.48 ± 23.44% (pCramoll). A análise com Live/Dead mostrou redução da morte celular de 65.04 ± 3.29% (H2O2) para 39.77 ± 2.93% (pCramoll) e 13.90 ± 9.01% (rCramoll). Os efeitos deletérios de H2O2 na proliferação celular foram reduzidos em 10.83% (pCramoll) e 24.17% (rCramoll). As lectinas atenuaram a produção excessiva de superóxido, o collapso do ΔΨm e os danos lisossomais e ao DNA das células Vero expostas à H2O2. Em conclusão nossos estudos demonstram que pCramoll e rCramoll possuem elevado potencial imunomodulador e citoprotetor.<br>This study aims to evaluate the immunomodulatory effects on macrophages and cytoprotector action against oxidative stress of Cramoll 1.4 (pCramoll) and rCramoll 1 (rCramoll). In the determination of the immunomodulory action, peritoneal macrophages from Balb/c mice were treated with different concentrations of lectins (0.625 to 10 mM) and we analyzed the effect on NO production (Griess Reagent), cell viability (MTT Reagent), induction of apoptosis (Kit Live/Dead and Acridine orange), superoxide anion production (MitoSOX), changes in mitochondrial membrane potential (ΔΨm) and phagocytosis of Staphylococcus aureus. The production of proinflammatory cytokines (IL-1β, IL-6, INF-γ e TNF-α) was analyzed in S. aureus infected and non-infected macrophages. Both lectins significantly enhanced Macrophages NO production and cytokines. The lectins were not cytotoxic as observed by MTT assay. However Live/Dead analysis revealed an increase of apoptosis in treated cells, the reduction of lysosomal activity was also reduced. The superoxide production was stimulated by both lectins, which was confirmed with the reduction on ΔΨm. S. aureus phagocytic activity of macrophages were enhanced in 27.1% and 22.47% by pCramoll and rCramoll, respectively. Finally, pCramoll and rCramoll downregulated the production of IL-6 and TNF-α and upregulated the expression of IL-1β, INF-γ during S. aureus infection of macrophages. In addtion, the protective effects of lectins against cell death induced by oxidative stress were evaluated. For this purpose, Vero cells (monkey kidney fibroblasts) were pretreated with increasing concentrations of lectins (0.625 to 10 μM) for 30 minutes and then were exposed to H2O2 (1mM). After 24 hours, the cytoprotective effect was evaluated and the cellular mechanisms involved were determined by flow cytometry involving: protection against cell death (Live/Dead kit), damage to lysosomes (Acridine Orange) and DNA (TUNEL), superoxide anion production (MitoSOX), changes in mitochondrial membrane potential (ΔΨm) (Rhodamine 123) and cell proliferation. pCramoll and rCramoll significantly attenuated the H2O2-induced cytotoxicity in a dose-dependent way, the maximum protective effects were 96.85 ± 15.59% (rCramoll) and 59.48 ± 23.44% (pCramoll). The Live/Dead analysis showed a reduction in apoptotic cells from 65.04 ± 3.29% to 39.77 ± 2.93% (pCramoll) and 13.90 ± 9.01% (rCramoll). The deleterious effects of
H2O2 on cell proliferation were reduced 10.83% (pCramoll) and 24.17% (rCramoll). The lectins attenuated the excessive superoxide production, the collapse of ΔΨm, lysosomal and DNA damage that occurred in Vero cells exposed to H2O2. In conclusion, our results show that pCramoll and rCramoll have high immunomodulatory potential on macrophages and cytoprotective effects against H2O2.
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Barreiro, Portela Esther. "Study of reactive oxygen species (ROS) and nitric oxide (NO) as molecular mediators of the sepsis-induced diaphragmatic contractile dysfunction : protective effect of heme oxygenases." Doctoral thesis, Universitat Pompeu Fabra, 2002. http://hdl.handle.net/10803/7066.
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Protein nitration is considered as a marker of reactive nitrogen species formation. Heme oxygenases (HOs) are important for the defence against oxidative stress. We evaluated the involvement of the neuronal (nNOS), the endothelial (eNOS), and the inducible (iNOS) in nitrotyrosine formation and localitzation, and both the expression and funcional significance (HO inhibition and contractility studies) of HOs in sepsis-induced muscle contractile dysfunction. Sepsis was elicited by injecting rats and transgenic mice deficient in either nNOS, eNOS, or iNOS isoforms with E.Coli lipolysaccharide (LPS). Nitrotyrosine formation and HO expressions were assessed by immunoblotting. Oxidative stress was assessed measuring protein oxidation, lipid peroxidation, and muscle glutathione. We conclude that protein tyrosine nitration occurs in normal muscles, and sepsis-mediated increase in nitrotyrosine formation is limited to the mitochondria and membrane muscle fractions. The iNOS isoform is mostly involved in nitrotyrosine formation. HOs protect normal and septic muscles from the deleterious effects of oxidants.<br>En un model de sepsi de disfunció diafragmàtica, s´ha avaluat el paper de les sintetases de l'òxid nítric (NOS) en la formació i localitzacio de 3-nitrotirosina, i l´expressió i significat biològic de les hemo oxigenases (HOs) (inhibidor de les HOs i estudis de contractilitat) davant l' estrès oxidatiu. La sepsi s'induí mitjançant injecció de 20 mg/kg del lipolisacàrid (LPS) d´Escherichia Coli a rates, i a ratolins deficients en les NOS induïble (iNOS), neuronal (nNOS) i endotelial (eNOS). Les proteïnes nitrificades i les HOs es van detectar amb anticossos específics. L' estrès oxidatiu s' avaluà mitjançant l' oxidació proteica, la peroxidació lipídica i el glutation muscular. Concloem que hi han proteïnes nitrificades en el múscul normal i aquestes s'incrementen durant la sepsi en les fraccions mitocondrial i membranar. L'isoforma iNOS és majorment responsable de la formació de nitrotirosina. Les HOs protegirien el múscul normal i sèptic dels efectes deleteris dels oxidants.
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Čangelová, Katarína. "Studium možných aplikací polymeru kyseliny glutamové." Master's thesis, Vysoké učení technické v Brně. Fakulta chemická, 2019. http://www.nusl.cz/ntk/nusl-401873.
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The subject of the thesis is study of possible applications of isoform of glutamic acid polymer (-PGA). The theoretical part is focused on the properties of this biopolymer and potential applications in various areas. Producers and mechanisms of biosynthesis are also mentioned. In the experimental part, the polymer was firstly characterised by following methods: FT-IR spectroscopy, TGA, DSC and SEC-MALS. Its isoelectric point, antimicrobial activity and solubility in various solvents were also determined. The biopolymer was also precipitated by divalent cations and its interaction with oppositely charged CTAB surfactant was studied. The main experimental study was researching the effect of -PGA on viability of Saccharomyces cerevisiae and Lactobacillus rhamnosus under stress conditions by flow cytometry. The performed stresses included ethanol exposure, high temperature and freezing stress, in which its effects were compared to conventional cryoprotectants. The cells of the mentioned microorganisms were also stressed osmotically and exposed to model gastrointestinal juices - gastric, pancreatic and bile. The protective effects of -PGA on the cells were recorded in ethanol stress on Lactobacillus rhamnosus. Its excellent cryoprotection properties were confirmed and its protective effect of gastric juice exposure on Saccharomyces cerevisiae cells was also observed. At the end of the experimental part, -PGA/alginate beads suitable for encapsulation of probiotic bacteria and -PGA/chitosan nanoparticles for encapsulation of biologically active substances.
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Risdon, Sydney. "Consommation d’édulcorants intenses non-caloriques et santé cardiométabolique : effets sur le contrôle glycémique et la fonction vasculaire chez le rongeur Sucralose and cardiometabolic health: current understandingfrom receptorsto clinical investigations Artificial sweeteners impair endothelial vascular reactivity: Preliminary results in rodents Is fasting blood glucose a reliable parameter to investigate the effect of non-nutritive sweeteners on glucose metabolism? Digestive n-6 Lipid Oxidation, a Key Trigger of Vascular Dysfunction and Atherosclerosis in the Western Diet: Protective Effects of Apple Polyphenols." Thesis, Avignon, 2021. http://www.theses.fr/2021AVIG0719.
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Les édulcorants ont été progressivement introduits dans l'alimentation humaine dans le but, de réduire l'apport calorique mais aussi de limiter les répercussions sur les niveaux de glycémie, tout en préservant le gout sucré, élément essentiel du plaisir gustatif. Plusieurs travaux de recherche ont néanmoins suggéré, contrairement aux intentions premières, que cette consommation d’édulcorants quotidienne pouvait participer à augmenter le risque de devenir obèse ou diabétique mais aussi le risque de mortalité cardiovasculaire. Dans ce contexte, l’objectif de ce travail de thèse a été d’identifier les effets d’une consommation chronique de boissons contenant des édulcorants de synthèse et non caloriques, seuls ou en synergie, sur le contrôle glycémique et la physiologie vasculaire, afin de comprendre le risque accru d’évènements cardiovasculaires observé chez les consommateurs fréquents d’édulcorants. Ainsi, nous avons pu mettre en évidence chez le rongeur la sensibilité du tissu vasculaire à l’exposition de l’acésulfame de potassium (Ace-K) et du sucralose, sensibilité qui semble indépendante de l’activation des récepteurs du gout sucré. De manière intéressante, les effets vasomoteurs de ces édulcorants sont apparus antagonistes l’un envers l’autre. Les études actuelles suggèrent également l’implication des édulcorants dans la survenue de facteurs de risque cardiovasculaire tel que l’obésité. Toutefois dans notre modèle, la consommation de sucralose dans le cadre d’un régime gras a permis au contraire de limiter les altérations de ce régime sur l’accumulation de tissu adipeux et sur le contrôle de la glycémie, mais également de potentialiser la réponse vasodilatatrice artérielle chez les souris. Ainsi, nos résultats démontrent l’importance d’identifier les conséquences propres directes (sur les cellules du tissu vasculaire) et indirectes (modulation des facteurs de risque cardiovasculaires) de chaque molécule sur la physiologie vasculaire. Néanmoins, des études supplémentaires sont nécessaires afin d’évaluer les effets spécifiques de chaque molécule sur cette balance vasomotrice<br>Artificial sweeteners have been extensively introduced into human diets with the objective of decreasing caloric intake and normalize the levels of blood glucose, while preserving an essential element of taste pleasure, the sweet taste. Nevertheless, several studies have suggested that a daily and sustained consumption of sweeteners could contribute to the increased risk of becoming obese or diabetic but also to the increased cardiovascular mortality risk. In this context, the objective of this work was to identify the effects of chronic consumption of beverages containing synthetic and non-caloric sweeteners on glycemic control and vascular physiology. Thus, we were able to demonstrate in rodents the sensitivity of vascular tissue to acesulfame potassium (Ace-K) and sucralose exposure that appears to be independent of sweet taste receptor activation. Interestingly, the vasomotor effects of these artificial sweeteners appeared to be antagonistic to each other. Current studies also suggest the involvement of artificial sweeteners in the occurrence of cardiometabolic disease such as obesity. Surprisingly, in our model, the consumption of sucralose appears to limit the deleterious effects of a high fat diet on body composition and glycemic control. The sucralose consumption even potentiated the vasodilatory arterial response in our mice model. Thus, according to the effects observed on glucose homeostasis, our results demonstrate the importance of identifying the specific direct (on vascular tissue cells) and indirect (modulation of cardiovascular risk factors) consequences of each molecule on vascular physiology. Nevertheless, further studies are needed to evaluate the specific effects of each molecule on this vasomotor balance
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Prins, Anneke. "The protective role of oryzacystatin-1 under abiotic stress." Diss., 2003. http://hdl.handle.net/2263/24479.
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One of the most important photosynthetic enzymes in a plant is ribulose-1,5¬bisphosphate carboxylase/oxygenase (Rubisco), which plays a key role in carbon fixation. Degradation of this enzyme leads to decreased carbon fixation and poor photosynthetic performance by the plant. It is therefore of interest to investigate possible ways of protecting this enzyme during stress conditions in order to generate plants that would perform better under extreme climates. In this study the effect of an expressed, exogenous rice cysteine proteinase inhibitor (OCI) in transformed tobacco plants on Rubisco stability/content under chilling and senescence was investigated. Results showed that there is no significant protective role for exogenous OCI on the degradation/content of Rubisco when tobacco plants were exposed to chilling. This result was found using native gel-based quantification procedures, as well as immuno-blotting, spot densitometric analysis, and a radioactive quantification assay as analysis techniques. The study, however, provided evidence for protection of Rubisco against degradation by expression of OCI under a more severe stress condition, such as senescence using native gel-based quantification procedures as detection techniques. Tobacco plants were also transformed with a newly designed vector allowing expressed OCI to be transported to the chloroplast. Failure to detect so far any OCI-¬expressing transformed plants and the idea that delay of senescence could prove beneficial to farmers by providing a more nutrient-dense crop with higher tolerance against stress-induced cell death are discussed.<br>Dissertation (MSc(Botany))--University of Pretoria, 2006.<br>Plant Science<br>unrestricted
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Jian, Bo-Lun, and 簡伯倫. "Study on the Protective Effect of Lipoic Acid under Hyperthermia and Hypoxia Stress." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/e2fs6v.
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碩士<br>國立高雄大學<br>運動健康與休閒學系碩士班<br>100<br>In this study, we evaluate the protective effects of lipoic acid under hyperthermia and hypoxia stress in mouse skeletal cell line (C2C12).The mature myotube were differentiated from C2C12 cells growth on differentiated medium containg 10% horse serum culture medium for 3-5 days. The results of western blotting show the level of Hsp70 was increased and lipoic acid enhanced the expression of Hsp70 under hyperthermia stress in myotubes. Moreover, the expression of Hsp70 also increased under 10% and 1% oxygen stress in myotubes.The other hand, the level of CXCR4, phosphorylated-p38 and Hsp70 proteins were also increased and the expression of Bcl-xL protein was decreased under hypoxia stress in myotubes. Furthermore, the expression of Bcl-xL protein was elevated and expression of phosphorylated-p38 protein was attenuated after administration of lipoic acid under hypoxia stress in myotubes. According to our results, it may indicate lipoic acid could against the injury of hypoxia stress by elevated the expression of Bcl-xL protein and attenuated the expression of phosphorylated-p38 protein in myotubes.
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Jiuan-Jen and 徐娟珍. "Protective effect of Occimum Grastissimum L. extracts on the oxidative stress-induced neurodegeneration." Thesis, 2007. http://ndltd.ncl.edu.tw/handle/03777653931408131050.
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碩士<br>中山醫學大學<br>生化暨生物科技研究所<br>95<br>Ocimum Gratissimum L. (OGL), containing various antioxidative components, is usually used as one of popular health protective medicines in Taiwan. In this study, we investigated the protective effect of OGL extracts on the H2O2-induced neurodegeneration. By using PC12 cells as a cell model, after pretreatment with various doses of OGL (50μg/ml, 125μg/ml, 250μg/ml and 500μg/ml ) for 1 hour, we then treated various doses of H2O2 (0.5mM, 1mM and 2mM). Since the blebbing was observed in the 2mM H2O2–treated group after 4 hour treatment, but not in the other groups (0.5mM and 1mM H2O2-treated groups), we used these two doses (0.5mM and 1mM H2O2) for the subsequent protective examinations of OGL extracts. The results showed that although both 0.5mM and 1mM H2O2 inhibited the catalase activity after 24 hours treatment, only 1mM H2O2 decreased cell viability. When pretreated with OGL extracts, these phenomenon were recovered in a dose-dependent manner. These data indicated that the OGL extracts may have the protective effect in the oxidative stress-induced neurodegeneration.
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Yi-WeiChen and 陳一瑋. "Protective effect of 3, 4-methylenedioxyphenol (sesamol) on stress-related mucosal injury in rats." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/21935269889836462912.
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碩士<br>國立成功大學<br>環境醫學研究所<br>99<br>Patients with stress-related mucosal disease have higher morbidity and mortality than the others at intensive care unit. 3,4-Methylenedioxyphenol (sesamol) has potent antioxidative and anti-inflammatory effects. The aim of this study is to investigate the effect of sesamol on water immersion restraint (WIR)-induced stress-related mucosal disease in rats. Rat gastric ulcer and hemorrhage were induced by WIR. The validation of WIR was tested first. For protective effect of sesamol, rats were pretreated orally with various doses of sesamol (0.1, 0.3, or 1 mg/kg) 30 min before WIR. Restrained on restraint board at 25℃ for 4 h induced severe ulcer and hemorrhage. Social support effect did not affect the induction of stress ulcer. WIR increased gastric mucosal ulcer and hemorrhage, tumor necrosis factor (TNF)-?, interleukin (IL)-1?, and IL-6 levels, compared with non-WIR group, but failed to affect mucosal lipid peroxidation and mucus secretion. Sesamol significantly decreased gastric ulceration and hemorrhage, decreased mucosal tumor necrosis factor ? (TNF-??, interleukin 1???IL-1??, and interleukin 6 (IL-6) productions, and increased interleukin 10 (IL-10), compared with WIR control group. Sesamol inhibited nuclear factor-?B (NF-?B) activity in sesamol-treated groups compared with WIR control group. In addition, increased myeloperoxidase (neutrophil marker) and CD68 (macrophage marker) levels in gastric mucosa were found in WIR-treated rats. Sesamol significantly decreased CD68 levels but not myeloperoxidase in mucosa compared to WIR-control groups. We hypothesize that sesamol protects against stress-related mucosal disease by inhibiting gastric mucosal proinflammatory cytokines production in rats.
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Huang, Ming-Yuan, and 黃銘瑗. "Protective Effect of Creatine Supplementation on Oxidative Stress Mediated Brain-type Creatine Kinase Depletion." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/81760711070364132410.
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碩士<br>國防醫學院<br>微生物及免疫學研究所<br>101<br>The generation of reactive oxygen species (ROS) will affect cellular homeostasis and high level of ROS are believed to be associated with cell death, disease, and aging. Aging results in progressive functional losses crossing multiple systems. Aging-induced hearing loss (AHL) may be contributed by ROS damage in the inner ear. In addition, the molecular mechanism for noise-induced hearing loss (NIHL) also involves the ROS formation. Cochleae are more vulnerable to oxidative stress compared to other organs because of the highly metabolic demands on their mechanosensory hair cells in response to sound stimulation. We recently showed that patients and mice with Huntington’s disease (HD) have hearing impairment and that the dysregulated phosphocreatine (PCr)‐creatine kinase (CK) system may account for this auditory dysfunction. Dietary creatine supplements have been shown to rescue the expression of cochlear brain type creatine kinase (CKB) in HD mice by reducing oxidative stress and thereby restoring their hearing. Thus, in my research, we hypothesize that dysregulated CKB not only be responsible for HD-related hearing impairment, but may also be implicated in several hearing impairments. We would like to investigate whether CKB plays an important role in ROS resultant hearing damages. Our results demonstrate that the expression of CKB in the cochlea would be reduced following the noise exposure or aging. Creatine supplementation helps in upregulating the expression of CKB in the mice cochleae. In addition, we showed that creatine, as an antioxidant, was demonstrated to protect auditory cells from ROS damage in vitro.
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Ke, Deng-Yi, and 柯登議. "Oxidative Stress Response of Cultured Cells to Model Protective Effect of Enzyme Hydrolysates from Hard Clam." Thesis, 2005. http://ndltd.ncl.edu.tw/handle/07741871742175035727.
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碩士<br>國立臺灣海洋大學<br>食品科學系<br>93<br>Previous studies demonstracted that hot water extract of fresh hard clam showed not only proliferation but also anti-tumor activity. The hydrolysates inhibited on hemoglobin-induced linoleic acid peroxidation, scavenging DPPH radical and reducing power. The aims of this study were to evaluate the protective effect of hydrolysates from hard clam by enzymeatical hydrolysis against pro-oxidant (AAPH, hydrogen peroxide, t-BHP and Cu2+) induced oxidative damage on cell culture. In the study, hydrolysates of Alcalase promote the phagocytosis by NBT test. Pro-oxidant can induce DNA fragmentation and decrease cell viability. Hydrolysates could chelate Cu2+ to protect against transition metal ion-induced cell line cytotoxicity and increase cell viability. Hysrolysis with Alcalase improved the capability of hard clam to inhibit the lipid oxidation as well as retard propagation of the oxidation process. AAPH induced cell oxidative stress and decrease cell viability. Hydrolysate of Protamex exhibited activity to scavenge free radical generated from AAPH. When cell were growth for 12h in the of AAPH and hydrolysate（500 �慊/ml）, the cell injury was inhibited by increasing cell viability, diminish ROS production. Our results presumed that the protection of pro-oxidant was decreased the ROS production and increased cell viability.
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Huang, Jhao-Wei, and 黃詔威. "An Investigation into the Protective Effect of Mannitol Against Oxidative Stress in the Retinal Pigment Epithelium." Thesis, 2006. http://ndltd.ncl.edu.tw/handle/85013027474037422659.
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碩士<br>國立陽明大學<br>藥理學研究所<br>94<br>The main purpose of this research was to investigate whether an osmotic/ anti-glaucoma agent mannitol could act as a neuroprotectant in the human retinal pigment epithelium (RPE) subjected to an oxidative stress.
As shown by the 3-(4,5dimethylthiazol-2-yl) 2,5-diphenyltetrazolium bromide (MTT) and trypan blue exclusion assays, mannitol dose-dependently attenuated the decreased cell viability of human RPE cells caused by incubating with H2O2 (500 μM, 1 mM and 10 mM). Presently, 1 mM mannitol increased the cell viability by 10 % (MTT assay) and 20 % (trypan blue assay) respectively. This adverse effect of H2O2 was significantly attenuated by pretreatment of RPE cells with 1 mM mannitol. This protective effect was further microscopically confirmed in hRPE cell culture.
In the human RPE cells exposed to 1 mM H2O2-induced oxidative stress, 1 mM mannitol reduced the production of reactive oxygen species and lipid peroxides by 62 % and 38 % respectively.
Interestingly, added mannitol at 100 μM and 1 mM dose-dependently up-regulated the level of catalase, but did not affect that of manganese-superoxide dismutase (MnSOD). In the present study, added 1 mM mannitol increased the level of catalase by 85 % as compared to that reflected by 1 mM H2O2 alone. These data have suggested that mannitol might protect the H2O2-induced damage to RPE cells by stimulating the up-regulation of catalase, but not MnSOD.
Taken together, this study has demonstrated a neuroprotective effect of mannitol in the human RPE cells subjected to an oxidative stress through above-mentioned mechanisms.
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Zhao, Fang. "Protective Effect of Peroxiredoxin 2 on Oxidative Stress Induced β-cell Toxicity in the Pancreatic β-cell Line MIN6". Thesis, 2011. http://hdl.handle.net/1807/31662.
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Type 1 and type 2 diabetes are characterized by an excessive loss of insulin producing β-cells. β-cells are particularly susceptible to increased oxidative stress induced apoptosis due to low expression of major antioxidants. Peroxiredoxin-2 (PRDX2) belongs to a group of antioxidants with antiapoptotic roles. Preliminary data indicate PRDX2 is expressed in the β-cells. Endogenous PRDX2 in the β-cell line MIN6 is found to decrease under oxidative stress conditions. I hypothesize that PRDX2 has a role in protecting β-cells against oxidative stress induced apoptosis. Overexpression or knockdown strategies were used to examine the role of PRDX2 in insulin-secreting MIN6 cells treated with various stimuli (cytokines, palmitate, streptozotocin) to induce apoptosis. Results showed that PRDX2 overexpression decreased oxidative stress induced apoptosis markers and cell death indicators, whereas knockdown of PRDX2 exaggerated oxidative stress induced toxicity. These findings suggest that PRDX2 plays a protective role in pancreatic β-cells under oxidative stress conditions.
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Voabil, Paula Cristina Antunes. "Protective effect of calcium dobesilate against inflammation and oxidative/nitrosative stress in the retina of a diabetic rat model." Master's thesis, 2010. http://hdl.handle.net/10316/28821.
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Dissertação de mestrado em Biologia Celular e Molecular apresentada ao Departamento de Ciências da Vida da Faculdade de Ciências e Tecnologia da Universidade de Coimbra.<br>A retinopatia diabética é uma das principais complicações da diabetes mellitus, sendo considerada uma das principais causas de perda de visão e cegueira em adultos em idade activa nos países desenvolvidos. O dobesilate de cálcio (CaD) é um derivado sintético do sulfonato de benzeno, utilizado no tratamento da retinopatia diabética. Clinicamente, a sua eficácia foi demonstrada, principalmente, através da correcção da excessiva permeabilidade vascular na retina em pacientes diabéticos e em diabetes experimental. Contudo, os mecanismos moleculares e celulares dos fármacos envolvidos nesses efeitos não estão ainda completamente esclarecidos. Os efeitos protectores do CaD podem estar relacionados com as suas propriedades antioxidantes ou, possivelmente, com uma acção anti-inflamatória. Assim, este estudo teve como principal objectivo elucidar o efeito do tratamento com o CaD na inflamação e no stress oxidativo/nitrosativo induzidos na retina pela diabetes, utilizando para isso um modelo animal de diabetes.
Ratos Wistar foram divididos em 4 grupos: controlos, animais tratados com CaD, diabéticos (2 meses de duração da diabetes) e diabéticos tratados com CaD (100 mg/kg/dia; administrado oralmente durante as duas últimas semanas). Devido à natureza inflamatória da retinopatia diabética, a reactividade glial foi avaliada nas células de Müller e nos astrócitos na retina. A expressão da proteína glial fibrilar acídica (GFAP) aumentou na retina aos 2 meses de diabetes. Curiosamente, o tratamento com CaD, por si só, fez aumentar os níveis de GFAP na retina. No que diz respeito à expressão das citocinas pró-inflamatórias, foi prestada particular atenção à interleucina-1β (IL-1β) e ao factor de necrose tumoral-α (TNF-α). Os níveis de expressão destas citocinas pró-inflamatórias aumentaram nas retinas dos animais diabéticos e o tratamento com CaD preveniu esse aumento. Além disso, o stress oxidativo/ nitrosativo foi avaliado através da detecção de grupos carbonilo oxidados e de resíduos de nitrotirosina. Tal com esperado, a diabetes aumentou o stress oxidativo/nitrosativo na retina, o qual foi inibido pelo tratamento com CaD, sugerindo assim que o efeito protector do CaD se mostra inegavelmente relacionado com suas as propriedades antioxidantes.
Em conclusão, estes resultados suportam resultados anteriores, mostrando que o CaD exerce efeitos protectores na retina, principalmente inibindo o stress oxidativo/nitrosativo e a inflamação. Particularmente, neste trabalho, foi demonstrada pela primeira vez a inibição da produção de citocinas pró-inflamatórias pelo CaD naretina. É também provável, que os efeitos protectores do CaD sejam essencialmente devido às suas propriedades antioxidantes.<br>Diabetic retinopathy is one of the most common complications of diabetes mellitus and is a leading cause of acquired blindness in working-age adults in developed countries. Calcium dobesilate (CaD) is a synthetic benzene sulfonate derivative used in the treatment of diabetic retinopathy. Its clinical effectiveness has been demonstrated mainly through a correction of the excessive vascular permeability in the retina of diabetic patients and in experimental diabetes. However, its molecular and cellular mechanisms of action are not completely elucidated. The protective effects of CaD might be due to its antioxidant properties or possibly they could also be related with an anti-inflammatory activity. Therefore, the main goal of the present study was to clarify the effects of the treatment with CaD on the inflammation and oxidative/nitrosative stress induced by diabetes in the retina of an animal model.
Wistar rats were divided into four groups: controls, animals treated with CaD, diabetic (2 month diabetes duration) and diabetic treated with CaD (100 mg/kg/day; orally given, during the last 2 weeks). Given the inflammatory nature of diabetic retinopathy, glial reactivity was evaluated in Müller cells and astrocytes. Glial fibrillary acidic protein (GFAP) immunoreactivity was upregulated in the retina at 2 months of diabetes. Interestingly, CaD per se also enhanced GFAP levels in the retina. Regarding the expression of pro-inflammatory cytokines, a particular attention was given to interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). The expression levels of these pro-inflammatory cytokines were elevated in the retinas of diabetic animals, and CaD was able to prevent this upregulation. Oxidative/nitrosative stress was analysed by the detection of oxidized carbonyl groups and tyrosine nitration. As expected, diabetes increased the oxidative/nitrosative stress in the retina, which was inhibited by treatment with CaD, thus suggesting that the protective effect of CaD appeared undeniably related with its antioxidant properties.
In conclusion, these results further support previous findings showing that CaD can exert potent protective effects in the retina, namely inhibiting oxidative/nitrosative stress and inflammation. In particular, the inhibition of the production of pro-inflammatory cytokines in the retina by CaD was demonstrated by the first time in this work. It is also likely that the protective effects of CaD are mainly due to its antioxidant properties.
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Hwang, Sun-Young. "Role of hyperhomocysteinemia in the regulation of oxidative stress and inflammatory responses in the kidney: protective effect of folic acid supplementation." 2011. http://hdl.handle.net/1993/5066.
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Hyperhomocysteinemia, a condition of elevated blood homocysteine (Hcy) level, is an independent risk factor for cardiovascular disease. Folic acid supplementation can effectively reduce blood Hcy levels. Recent studies have demonstrated that hyperhomocysteinemia is also associated with kidney disease. However, the underlying mechanisms remain unclear. The overall objective of the study was to investigate the biochemical and molecular mechanisms of Hcy-induced kidney injury and the effect of folic acid supplementation on Hcy-induced kidney injury.
Hyperhomocysteinemia was induced in Sprague-Dawley rats by feeding a high-methionine diet for 12 weeks. An elevation of serum total Hcy level was observed in hyperhomocysteinemic rats. Hyperhomocysteinemia-induced superoxide anion production via nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activation resulted in oxidative stress in the kidney. Reduction of oxidative stress by inhibiting superoxide anion production effectively ameliorated hyperhomocysteinemia-induced kidney injury.
Inflammatory responses such as increased chemokine expression have been implicated as one of the mechanisms of kidney disease. Monocyte chemoattractant protein-1 (MCP-1) is a potent chemokine that is involved in the inflammatory response in kidney disease. Nuclear factor-kappa B (NF-kappaB) plays an important role in upregulation of MCP-1 expression. We investigated the effect of hyperhomocysteinemia on MCP-1 expression and the molecular mechanism responsible for such an effect in rat kidneys as well as in human kidney proximal tubular cells.
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Liao, Yu-Ting, та 廖宇婷. "Protective effect of solid-state fermented crops by Ganoderma lucidum against oxidation stress and β-amyloid plaques induced damage in human neuron cells". Thesis, 2018. http://ndltd.ncl.edu.tw/handle/y5frm5.
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碩士<br>國立臺灣海洋大學<br>食品科學系<br>106<br>Alzheimer's disease is a neurodegenerative disease caused by the stacked of β-amyloid peptides. Our laboratory has established the culture medium and condition for the solid-state cultivation of G.lucidum mycelia. This study investigated the protective effect of solid-state fermented crops by G.lucidum against oxidation stress caused by H2O2 and Aβ25-35 in neuroblastoma SH-SY5Y cell line. Various extracts by 10% ethanol extraction using microwave (A), 70oC water extraction (B) and 100oC water extraction followed by ethanol precipitation (C) of G.lucidum fermented product were prepared and the bioactive contents were analyzed. The total glucan and triterpene contents for the 3 extracts were 6.27 – 60.73 g/100 g and 1.43 – 20.30 mg/g, respectively, with the extract C being the highest total glucan content, and the extract B the highest triterpene content. The extract A and B content the more GABA. Median inhibitory concentration for DPPH and ABTS scavenging activity for the all extracts were 6.24 – 10.61 and 8.07 – 11.14 mg/mL, respectively. Pretreatment of extract A significantly reduce the ROS concentration in SH-SY5Y cells. Pretreatment with extracts (10 – 500 μg/mL) followed by H2O2 (150 μM) or Aβ25-35 (10 μM) damage, significantly increased cell viability 6.22-30.64%. In addition, a significant increase in glutathione peroxidase (GPx) was observed in all extracts treated group and GABA standard at 50, 100 μg/mL. A high concentration of G.lucidum extract and 10 μM Aβ25-35 were used to simulate the damage of Alzheimer’s disease cells. Pretreatment with 100 μg/mL extract B could significantly enhance catalase (CAT), superoxide dismutase (SOD) and GPx activity by 1.33, 1.52 and 1.34 times compared to Aβ25-35 control group, respectively. In addition, extract B and C decrease the acetylcholinesterase (AChE) activity and malondialdehyde (MDA) content in neuron cells, respectively. Meanwhile, extract B (100 μg/mL) inhibits cell apoptosis to protect
neuron cells from H2O2- and Aβ25-35-induced damage.
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Li, Chiew Siau, and 丘曉莉. "Dietary administration of Gracilaria tenuistipitata extract containing diets enhanced the immune response of white shrimp Litopenaeus vannamei and its protective effect against ammonia stress." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/25508105569856957281.
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碩士<br>國立臺灣海洋大學<br>水產養殖學系<br>99<br>Immune parameters such as haemogram, phenoloxidase (PO) activity, respiratory burst (RB), superoxide dismutase (SOD) activity, lysozyme activity and haemolymph protein were examined after the white shrimp Litopenaeus vannamei had been fed diets containing the hot-water extract of red alga Gracilaria tenuistipitata at 0, 0.5, 1.0 and 2.0 g kg1 for 7, 14, 21 and 28 days. These parameters increased directly with the amount of extract in diet. The haemocyte count, RB, SOD activity reached the highest levels after 14 days, whereas PO activity and lysozyme activity reached the highest levels after 28 days. In a separate experiment, L. vannamei which had been fed diets containing the extract for 3 weeks, were exposed to 5 mg l1 ammonia-N for 6, 12, 24, 72, 120 h. The immune parameters of shrimp exposed to ammonia-N dropped to the lowest in 6 h. The immune parameters of shrimp fed the extract-containing diets returned to the background value earlier, than did those of shrimp fed the control diet. Haemocyte count, PO activity and RB of shrimp fed 2.0 g kg1 diet returned to the background value after 24 h, 12 h and 6 h, respectively. The SOD activity and haemolymph protein of shrimp fed 2.0 g kg1 diet returned to the background value after 24 h. Lysozyme activity of shrimp fed 0.5, 1.0 and 2.0 kg1 diet returned to the background value after 12 h. In the challenged test, white shrimp L. vannamei which had been fed diets containing the extract after 2 weeks, were challenged with V. alginolyticus and WSSV at 2 × 106 cfu shrimp1 and 1 × 103 copies shrimp1, respectively, and then placed in seawater. The survival rate of shrimp fed the extract-containing diets was significantly higher than that of shrimp fed the control diet at 72-144 h post-challenge. It was concluded that L. vannamei fed the hot-water extract of G. tenuistipitata at 2.0 g kg1 or less showed increased immunity as well as protective immune response against ammonia stress, and increased resistance to V. alginolyticus and WSSV.
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Killian, Brittany, and 柯昀君. "The Association of Heavy Metal Exposure and Oxidative Stress on Kindergarten Children Living near the No.6 Naphtha Cracking Plant and the Potential Protective Effect of Dietary Antioxidant Intake on Oxidative Damage." Thesis, 2017. http://ndltd.ncl.edu.tw/handle/e6bb2z.
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碩士<br>國立臺灣大學<br>公共衛生碩士學位學程<br>105<br>Background: Air pollution is believed to cause harmful human effects in part through the mechanism of oxidative stress. Oxidative stress occurs when there is an imbalance between oxidants and antioxidants in the body, and it is associated with many human health effects, including respiratory diseases, chronic diseases, and overall mortality and morbidity. Heavy metals, present in particulate matter linked to industrial complexes, have been hypothesized as a cause of oxidative stress. Children are particularly vulnerable to oxidative stress, with potential health effects ranging from respiratory disease to neurological damage. Researchers recently have hypothesized that dietary antioxidant intake might provide a protective effect against oxidative stress.
Objective: The objective of this study is to investigate the social determinants of health of nutritional and pollution status, to determine whether dietary antioxidant intake plays a protective role in preventing oxidative damage, and to assess whether oxidative stress is positively associated with heavy metal exposure in kindergarten children living near a petrochemical complex in Yunlin County, Taiwan.
Methods: 168 children ages 4-8 were recruited, 87 from the pre-determined high exposure area and 81 from the pre-determined low exposure area. This cross-sectional study used a specially-developed semi-quantitative food frequency questionnaire (FFQ) to assess the participants’ intake of antioxidants, overall dietary patterns, and socioeconomic characteristics. A morning spot urine sample was collected from each participant at the same time as the FFQ. The FFQ was analyzed with nutritionists to determine each participant''s’ total antioxidant intake per week. The urine samples were analyzed using Inductively coupled plasma mass spectrometry (ICP-MS) and liquid chromatography mass spectrometry (LC-MS) to find concentrations of eleven heavy metals and four biomarkers for oxidative stress. ANCOVA tests were performed to determine between-group differences in socioeconomic, dietary, and exposure variables. Multiple linear regression was performed to determine significant predictors of urinary oxidative stress.
Results: ANCOVA tests revealed significant differences in urinary 8-OHdG and eight heavy metals (g/g-creatinine) between the high and low exposure group, with the high exposure group’s average concentrations higher than the low exposure group’s. Weighted average distance of the participants’ home and kindergarten addresses to the exposure site was a significant predictor of urinary heavy metal concentrations. Dietary differences were observed but they were not statistically significant. Multiple linear regression tests showed higher urinary heavy metal concentrations associated with higher urinary 8-OHdG. Increased total antioxidant intake per week (mmol/g) resulted in a decrease in urinary 8-OHdG, but these results were not statistically significant.
Conclusion and Recommendations: This study provided data on the associations between socioeconomic factors, air pollution, and nutrition. Heavy metals and oxidative stress were higher in the group living closer to the petrochemical plant, indicating an increased risk of exposure. Dietary antioxidant intake was associated with lower oxidative stress, but these results were not statistically significant, indicating that the current dietary intake of antioxidants, which is lower than average, is not enough to protect this population from urinary oxidative stress. It is recommended that further studies be done on this population to determine if a higher intake of dietary antioxidants would provide a protective effect against oxidative stress, as well as investigate other sources of oxidative stress besides heavy metal exposure. In addition, stricter regulation of industrial pollution to reduce exposure for the study population is also recommended.
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Pattanawong, Tarnrat. "Protective Effects of Selected Phenolic Compounds on Oxidative Stress." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/5w37jt.
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碩士<br>嘉南藥理大學<br>保健營養系<br>102<br>The aim of this study was to evaluate the effect of selected phenolic compounds on oxidative stress. The phenolic compounds in the range of 50-500 µg/ml showed no cytoxicity in the growth of HepG2 cells except Chrysin, Flavones, Galangin, and Baicalein.Flavonols, such as Quercetin, Morin, Myricetin, Rutin, Fisetin, and Kaemferol, and some phenolic acids such as Caffeic acid, and Chlorogenic, show greater protection on in the growth of HepG2 cells induced by 0.1 mM t-BHP than flavones, such as Chrysin, Baicalein, Apigenin, Nobilelin, and Tangeretin. For ROS generation, Quercetin, Morin, Myricetin, Rutin, Fisetin, Kaemferol, and Caffeic acid showed significant protection in these models. For mitochondrial membrane potential tests, Quercetin, Morin, Myricetin, Fisetin, Kaemferol, Caffeic acid and Chlorogenic acid showed significant protection mitochondrial membrane potential in these models. For the acellular tests, Quercetin, Morin, Myricetin, Rutin, Fisetin, Kaemferol, Caffeic acid, and Chlorogenic acid increased SOD activity and the inhibition of DPPH and NO. In cellular and acellular model systems, Quercetin, Morin, Myricetin, Rutin, Fisetin, Kaemferol, Caffeic, and Chlorogenic demonstrated significantly inhibitory effect on oxidative stress due to their remarkable antioxidant activity.
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Chiang, Chun-Hsien, and 江俊嫻. "Eicosapentaenoic acid has protective effects against oxidative stress in cardiomyocytes." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/39724372813677467195.
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Li-ChingLin and 林莉卿. "The underlying Mechanism of Companions’ Protective effects Against Stress-decreased Neurogenesis." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/97058435517558717425.
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Huang, Yu-Ting, and 黃鈺婷. "Protective Effects of Astaxanthin on Oxidative Stress- and Beta- Amyloid- Induced Neurotoxicity." Thesis, 2007. http://ndltd.ncl.edu.tw/handle/95413778516922266044.
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碩士<br>國立臺灣海洋大學<br>食品科學系<br>95<br>Abstract
Recently, oxidative stress has been implicated in the progression of Alzheimer’s disease and antioxidants may protect neural cells from this attack. Astaxanthin (AST) is a carotenoid found in marine animals and alga. Several previous studies have demonstrated that AST exhibits a wide variety of biological activities including antioxidant, antitumor effects. In this study prove 50 □M AST reduce DNA fragmentation caused by H2O2 through inhibition of about 50% of caspase activity and 41.5% of mitochondria transmembrane potential. Morover inhibition from 26.17% to 67.7% of beta-amyloid(A□) fibrils formation is with time dependent manner. Further 100 □M AST can inhibit neuroinflammation factor include NO release, Ca2+ influx and 50% of ERK phosphorylation.
In conclusion, AST may against H2O2-/A□- induced neurotoxicity through inhibiting apoptosis signalling pathway and reducing expression of neuroinflammation factor and protein. Furthmore, AST has potential on apply to prevent neurodegenerative disorders (EX: Alzheimer’s disease).
Keywords: Astaxanthin, Neuroprotection, Hydrogen peroxide, Amyloid-□, apoptosis, Neuroinflamation
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Lin, En-Yuan, and 林恩源. "Protective Effects of Polygonum Multiflorum Thunb ActiveIngredients on Oxidative Stress-Related Diseases." Thesis, 2019. http://ndltd.ncl.edu.tw/handle/7a2wr5.
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LEE, JUN-RU, and 李俊儒. "Development of oxidative stress damage model and protective effects of antioxidant agents in keratinocytes." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/39900368707857144921.
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碩士<br>中華醫事科技大學<br>生物科技研究所<br>95<br>The utilization of Radiometer to measure ultraviolet radiation in skin exposure assessment is limited since the lack of spectral irradiance and full wavelength scanning. An USB 4000 Miniature Fiber Optic Spectrometer was alternative used to measure the UVR emission and exposure dose from UV lamps. Following the measuring method, UVB induced oxidative stress in keratinocytes cell lines, xb-2 (mouse) and HaCaT (human), were establishes. This model was further applied to assess the protective effect of certain antioxidant agents.
After UVB 60 mJ/cm2 exposure and then incubation 24 hr was found as the half efficiency does (ED50) in preliminary test. Both mouse and human keratinocyte cell lines showed the cellular ROS (reactive oxygen species), extracellular LDH (lactate dehydrogenase) increased, and in coincidence with the cellular survival (MTT test) decrease under the condition of ED50. The effects of antioxidant agents such as ferulic acid, feruloyl oligosaccharides, and Vitamin C showed protective capacity in this model.
Based on the results from this study, the UVB exposure model could more accurately provides the information of spectrophotographies and UVB dosage. Moreover, the UV exposure model was evidenced to apply in evaluating the protective effect of antioxidant agents in keratinocytes.
Key word：keratinocyte、ultraviolet radiation、antioxidant agents oxidative stress、Spectroradiometer system
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Woo, Wai Hong Connie. "Role of hyperhomocysteinemia in liver injury and abnormal lipid metabolism (protective effect of folic acid supplementation)." 2007. http://hdl.handle.net/1993/2758.
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Hyperhomocysteinemia, a condition of elevated blood homocysteine level, is an independent risk factor for cardiovascular diseases. Folic acid can effectively reduce blood homocysteine levels. Recent studies have shown that hyperhomocysteinemia is also associated with liver disorders. However, the underlying mechanisms remain unclear. The general objective of my study was to investigate the biochemical and molecular mechanisms of homocysteine-induced liver injury and abnormal lipid metabolism.
Hyperhomocysteinemia was induced in Sprague-Dawley rats by feeding a high-methionine diet for 4 weeks. An elevation of serum aminotransferases activities (indicator for liver injury) and an increase in hepatic lipid peroxidation were observed in hyperhomocysteinemic rats. Hyperhomocysteinemia-induced superoxide anion production led to oxidative stress in the liver. Reduction of oxidative stress by inhibiting superoxide anion production ameliorated hyperhomocysteinemia-induced liver injury. A significant elevation of hepatic and serum cholesterol concentrations in hyperhomocysteinemic rats was observed, exclusively due to increased expression of HMG-CoA reductase in hepatocytes. The molecular mechanisms of homocysteine-induced adverse effects were further investigated in isolated rat hepatocytes and in human hepatoma cells (HepG2). Hcy stimulated HMG-CoA reductase expression in hepatocytes via activation of transcription factors, namely, sterol regulatory element-binding protein-2 (SREBP-2), cAMP response element binding protein (CREB) and nuclear factor Y (NF-Y). Activation of these 3 transcription factors was detected in hyperhomocysteinemic rat liver and in homocysteine-treated hepatocytes. Pretreatment of hepatocytes with inhibitors for individual transcription factors effectively attenuated Hcy-induced HMG-CoA reductase mRNA expression. Supplementation of folic acid in diet significantly reduced serum homocysteine level and effectively inhibited hyperhomocysteinemia-induced superoxide anion production, resulting in amelioration of oxidative stress-mediated liver injury in hyperhomocysteinemic rats. These results reflected a protective role of folic acid in hyperhomocysteinemia-induced liver injury.
In conclusion, the present study demonstrates that (1) hyperhomocysteinemia can cause oxidative stress and liver injury; (2) homocysteine stimulates cholesterol biosynthesis in hepatocytes via transcriptional regulation of HMG-CoA reductase expression; (3) supplementation of folic acid offers a hepatoprotective effect during hyperhomocysteinemia. Oxidative stress and accumulation of cholesterol in the liver contribute to liver injury associated with hyperhomocysteinemia. The role of folic acid in maintaining good health may extend beyond the cardiovascular system to encompass hyperhomocysteinemia-associated liver disorders.<br>October 2007
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Bu, So Young. "Bone protective effects of dried plum and its polyphenols under inflammatory and oxidative stress conditions." 2007. http://digital.library.okstate.edu/etd/umi-okstate-2223.pdf.
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Chen, Guan-Lin, and 陳冠霖. "Study on the Protective Effects of Lipoic Acid in Skeletal Muscle under Lipopolysaccharide Oxidative Stress." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/90064660382620176776.
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碩士<br>國立高雄大學<br>運動健康與休閒學系碩士班<br>99<br>In this study, we evaluate the anti-apoptosis pathway of lipoic acid under lipopolysaccha- ride oxidative stress in mouse skeletal cell line (C2C12). The mature myotubes were different- iated from C2C12 cells growth on 10% horse serum differentiation medium 3-5 days. The result of western blotting shows the level of phosphorylate Akt and Bcl-xL protein was incre- ased in the 5μM, 50μM and 0.5mM of lipoic acid treatment and the protein level was decreas- ed especially in 5mM and 10mM lipoic acid treatment. Therefore, the level of phosphorylate Akt and Bcl-xL protein was decreased at the 4, 5 hours treatment. It was shown the high dose and long-term treatment of lipoic acid may induce toxicity in myotubes, but low dose of lipoic acid may protect cells from damage. On the other hand, the phosphorylate Akt and Bcl-xL proteins were decreased by after treatment of lipopolysaccharide, especially in the dosage of 20μg/ml. Moreover, the level of TLR4 protein was expressed after lipopolysaccharide treatm- ent. These results show that oxidative stress of lipopolysaccharide in myotubes were induced by TLR4 protein and may induce oxidative stress by lower the express of phosphorylate Akt and Bcl-xL proteins. Furthermore, the level of Bcl-xL was inhibited after treatment with LY294002. It shows the express of Bcl-xL was regulated by p-Akt. Our results also show after treatment of lipopolysaccharide, lipoic acid can not affect the express of p-Akt and Bcl-xL in myotubes containing LY294002. According to our results, it shows that lipoic acid could against myotubes from oxidative stress by enhancing the express of p-Akt and Bcl-xL protein. It is indicated the lipoic acid against myotubes from lipopolysaccharide stress by PI3K/Akt pathway.
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Hsu, Po-sheng, and 許博勝. "The Effects of Wearing Encapsulating Protective Clothes (EPC), Workload and Environment Temperature on Heat Stress." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/15792684763958429180.
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碩士<br>朝陽科技大學<br>工業工程與管理系碩士班<br>101<br>Heat stress is well-known safety and health hazards, especially for workers wearing Encapsulating Protective Clothing (EPC) in high temperature environment. The body heat and sweat would form a micro-environment climate between the skin and EPC during EPC works. Currentenly, the monitoring of thermal exposure is still limited to the assessment of the external environment.
This research used personal heat stress monitor, Polar-rs800cx heart rate monitor, electronic scales, and subjective discomfort scale to explore the skin temperature, tympanic temperature, micro-environment temperature, heart rate, sweat rate, and subjective discomfort of six males under different external environment temperature (21℃ or 29℃), EPC wearing condition (not worn or worn), workload (moderate load or heavy load), and repetition (1st or 2nd). This study also compare the differences between the external and micro environments.
The results showed that the “external environment temperature” and “EPC wearing condition” have significant effects on skin temperature, tympanic temperature, heart rate, subjective discomfort, and micro-environment temperature. “Workload” showed significant effect on heart rate. “Repetition” showed significant effect on tympanic temperature and subjective discomfort. Significant differences between the external and micro environments were found in this study. The micro-environment temperatures were significantly higher than the external environment temperatures.
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Weng, Ching-Yi, and 翁靜儀. "Protective effects of ginseng essence on CCl4-induced oxidative stress and liver injury in rats." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/4d4jdm.
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碩士<br>國立臺灣大學<br>食品科技研究所<br>101<br>Liver is a vital organ, which is responsible for the regulation of nutrients metabolism, detoxification functions and others biochemical reactions. Many reaserches have reported that civilization diseases, such as chronic inflammation, and cancer are related to reactive oxygen species (ROS). Therefore, reducing free radicals maybe decrease the incidence of many diseases.
The major components of ginseng essence include four herbs, Panax quinquefolius, Panax ginseng, Nelumbo nucifera and Lilium longiflorum. Ginsenosides are major active compounds in ginseng essence, and have been reported as the active compounds of hepatoprotection, anti-obesity, anti-tumor, anti-diabetic, and anti-inflammatory effects in many researches.
Therefore, the objective of this study is to evaluate the hepatoprotective effect of ginseng essence on carbon tetrachloride (CCl4)-induced liver fibrosis in animal model, investigate the potential mechanism in the regulation of oxidative stress and determine the contents of acive compounds (ginsenosides) in ginseng essence.
In the CCl4-induced animal model male Wistar rats were randomized into six groups: (A) control group was only treated with vehicle; (B) negative control group was treated with CCl4; (C) positive control group was treated with CCl4 and silymarin (0.5 g/kg bw/day); (D) low dose group was treated with CCl4 and 0.625 g/kg bw/day ginseng essence; (E) medium dose group was treated with CCl4 and 1.25 g/kg bw/day ginseng essence; (F) high dose group was treated with CCl4 and 3.125 g/kg bw/day ginseng essence. Using oral administration of 20% CCl4 (1.5 ml/kg bw) induced chronic liver damage in rats. This experiment was performed for 9 weeks, including 8-week induction of CCl4. The effects of ginseng essence on liver function, oxidative stress and inflammation asseeement index in vivo were investigated.
In the results of determinations of active compounds, there are ginsenoside Rg1, Re, Rb1, Rc, Rd and Rg3 in ginseng essence. Three of them, ginsenoside Rb1, Rg3 and Rg1 have been reported to exert hepatoprotective effect by previous studies. In the results of animal experiment, all ginseng essence treatments stablely increase body weight as compared to negative control group. After induction of CCl4, negative control group have higher relative organ weight than control group. However, after the oral administration of ginseng essence can improve the inflammation in organs. Regarding liver function, ginseng essence can effectively descrease the activities of AST and ALT, and increase albumin in serum. Additionaly, ginseng essence can also descrease lipids in liver, and improve CCl4-induced abnormal metabolism of lipid. In the results of histopathological analysis, the oral administration of ginseng essence can reduce the score of liver damage. In terms of oxidative stress, as compared to carbon tetrachloride group, the oral administration of ginseng essence can also elevate the activities of antioxidative enzymes and the conten of antioxidant, and reduce the content of lipid peroxides. Moreover, CCl4 can cause hepatotoxicity, and results in inflammation and promote the production of inflammatory mediators. The oral administration of ginseng essence can descrease the content of pro-inflammation cytokine, such like TNF-α、INF-γ、IL-6 and TGF-β, as well as inhibit the activation of hepatic stallate cells.
In conclusion, ginseng essence could ameliorate the oxidative stress and inflammation to improve liver function and abnormal metabolism of lipid in CCl4–induced rats. Additionally, it could inhibit the activation of hepatic stallate cells by elevating the activities of antioxidative enzymes and the content of antioxidant, and then can ameliorate liver fibrosis. Therefore, ginseng essence could be a promising hepatoprotective product in the future.
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Chen, Yen-Wen, and 鄭彥文. "Construction of Real-time Personal Heat Stress Monitor used in Encapsulating Protective Clothing and the Effects of Wearing Encapsulating Protective Clothing on Hand Dexterity." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/44239854712095237644.
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碩士<br>朝陽科技大學<br>工業工程與管理系碩士班<br>97<br>Heat stress is a well-known industrial safety hazard that causes heat injury. It is more hazardous to those who have to wear Encapsulating Protective Clothing (EPC) during work. People doing this kind of jobs such as construction、refinement、asbestos purgation、chemical experiment、poison purgation or exact commercial foundry, have to wear Encapsulating Protective Clothing(EPC) while performing their tasks. Wearing EPC is easier to increase the heat from environment to human body, then, affect the worker’s health and productivity.
The heat stress monitor of the workers who don’t wear EPC is still limited to normal environment condition. If the heat stress is being underestimated, the workers would easily increase the risk of getting hurt by heat stress. If being overestimated, the control measures would probably lead to the reduction of productivity. We have to monitor the heat stress inside of microenvironment worn by workers and their physiology condition immediately and discuss the effect of wearing EPC to the dexterity.
The first research goal is to integrate a personal monitor. We can measure the microenvironment inside the EPC by using the temperature and wet sensors、heartbeat rate、tympanic thermometry and thermography. The second research goal is to compare the length of finishing time of pegboard tasks under three different situations “barehanded”, “gloved” and “gloved EPC” and see how it affects the dexterity.
The integrated personal monitor can be used to monitor the inside of EPC worn by workers, using SHT15 to estimate the climate of microenvironment, LM-92 to estimate the skin temperature、tympanic thermometry sensors-MLX90614 to estimate the ear temperature、POLAR S810 to estimate the physiology situation.The data will be shown immediately through a Borland C++ Builder 6.0 system. There is a big difference between the barehanded (45.97±5.87 s), gloved hand (127.36±47.96 s) and EPC worn (129.44±48.76’s) conditions. Furthermore, the dexterity of the bare hand is better than the other conditions.
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Chang, Simon, and 張肇恩. "Neuropsin inactivation has protective effects on depressive-like behaviours and memory impairments induced by chronic stress." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/hev8vj.
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Lin, Rung-Ying, and 林容瑩. "Protective Effects of Several Drugs on Ethanol-induced Gastric Oxidative Stress and Hemorrhagic Ulcer in Rats." Thesis, 2005. http://ndltd.ncl.edu.tw/handle/81243734824858845776.
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碩士<br>國立成功大學<br>藥理學研究所<br>93<br>Some compounds primarily have effects on immune, neural or even reproductive systems naturally occurring or synthetic in organisms and their effects on gastric damage are unknown. For instance: Lysozyme chloride possesses multiple pharmacological actions on various diseases. Melatonin has been well known as a free-radical scavenger. Estrogens play an important role in reproductive physiology. However, their actions on gastric mucosal protection have not yet been extensively studied. The aim was to study their effects on gastric oxidative stress and hemorrhagic ulcer in ethanol-treated rats.
Male Wistar rats weighing 260-320 g were deprived of food for 24 h followed by gastric surgical procedure. After gastric surgery, rat stomachs were irrigated for 3 h with acidified ethanol（20% ethanol in gastric juice ） or gastric juice. Drugs were challenged either intragastrically or intraperitoneally 30 min before acidified ethanol-irrigation. Aggravation of gastric acid back-diffusion, mucosal lipid peroxide generation and hemorrhagic ulcer as well as attenuation of mucosal glutathione levels, mucus production and blood flow（20 min later after ethanol administration ） was achieved in acidified ethanol-treated rats.
Lysozyme chloride inhibited these ulcerogenic parameters dose-dependently. Its effect on these offensive and defensive parameters was reversed by indomethacin. Melotonin, which has the most significant influences on enhancing the levels of glutathione and suppressing the generation of lipid peroxides, also reduced ulcer formation. Otherwise, the edema of gastric wall was occurred in the group treated with estrogen （β-estradiol）. Different time points, pretreatment or after surgery, of estrogen administration led to the diverse results. Pretreatment of estrogen suppressed most ulcerogenic parameters, except for the extent of acid-back diffusion and hemoglobin concentrations. Furthermore, an enhancement in mucosal blood flow was obtained 5 to 20 minutes after estrogen had been administered. Unexpectedly, indomethacin treatment released rat stomachs from ethanol attack. The depression of hemoglobin, histamine and mucus levels was observed in the administration of this anti-inflammatory drug .
In conclusion, these drugs improve ethanol-induce hemorrahagic ulcer through distinct mechanisms. Lysozyme chloride-ameliorated gastric hemorrhagic ulcer is through its antioxidant and prostaglandin stimulating effect. Melatonin protects against ulceration by stimulating mucosal glutathione, PGE2 biosynthesis, mucus production and scavenging oxyradicals. Estrogen exerts gastroprotection via enhancing the mucosal blood flow.
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Hsieh, Ming-Chou, and 謝明洲. "Protective Effects of Ascophyllum nodosum Extract on Cisplatin-induced Spermatogenic Damage and Oxidative Stress in Hamsters." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/33786214541591766511.
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碩士<br>國立臺灣海洋大學<br>食品科學系<br>98<br>Oxidative stress is now recognized as a common pathology that affects up to half of all infertile men. This study extracted powder of Ascophyllum nodosum by ethanol, acetone, supercritical fluid extract (SFE) and ethanol SFE respectively, and obtained ANE, ANA, ANS and ANC. ANA contained the most fucoxanthin content. And ANE contained the highest level of total polyphenolic content, also demonstrated the strong DPPH radical scavenging activity and reducing power. The ANE, ANA, ANS and ANC did not exert any cytotoxic effect on RAW264.7 under the tested concentration (200 ug/mL). Four kind of extracts remarkablely decreased superoxide anion and intracellular ROS content of macrophage induced by LPS. To evaluate the protective effects of ANE against Cisplatin (CP) -induced reproductive toxicity in hamsters. ANE reduced the extent of CP-induced sperm concentration, abnormality and enhanced sperm motility and mitochondrial membrane potential. Treatment with ANE restored the control level of malondialdehyde (MDA) and intracellular reactive oxygen species (ROS) in the CP-treated testis. The CP injection also induced decline in the levels of superoxide dismutase (SOD) were significantly reversed to control levels in groups where CP was preceded by the administration of ANE. Our results showed the histopathological findings of testes in short term treatment. This study clearly indicates that CP-treatment impaired markedly testicular function, and ANE treatment increased the activities of testicular antioxidant enzymes and restored sperm characteristics. The possible potential beneficial effects of ANE were particularly focused on fucoxanthin, total polyphenol and flavonoid compounds. In our studies, ANE have been shown to exhibit strong antioxidant activity which is attributed to quenching and scavenging free radicals. The protective effects of tested brown algae extract are, therefore, suggested to be mediated by their potent antioxidant activities, and provided significant amelioration of oxidative stress parameters.
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Walker, Kimberly Marie. "The protective effect of social support on student engagement for high school students experiencing dating abuse." Thesis, 2011. http://hdl.handle.net/2152/ETD-UT-2011-12-4437.
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The purpose of this study is to examine the role of social support as a moderator between dating abuse and student engagement. Informed by the positive youth development perspective and the stress-buffering model, this study will examine the effects of dating abuse victimization on student engagement and the buffering role of social support in that relationship. Specifically, this study will use self-report measures from a rural/semi-rural, high school sample and multiple regression analysis to determine the effect of dating abuse on student engagement. If a significant relationship is found between dating abuse and student engagement, this study will then use multiple regression analysis to determine the moderating effect of social support on the relationship between dating abuse and student engagement. Research on the protective effects of social support on student engagement is critical to the design and implementation of interventions which have the potential to significantly improve the health, mental health, social, and education outcomes for adolescents who have experienced dating abuse.<br>text
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Lin, Hui-Mei, and 林卉梅. "Protective effects of the fruit of Ligustrum lucidum on acute butylated hydroxytoluene-induced oxidative stress in rats." Thesis, 2006. http://ndltd.ncl.edu.tw/handle/25691300887662819577.
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碩士<br>高雄醫學大學<br>天然藥物研究所碩士班<br>94<br>Nüzhenzi (NZZ) is a dry fruit of Ligustrum lucidum Ait. (Oleaceae) that applied as tonic for kidney, liver and commonly prescribed in traditional Chinese medicine. The aim of this study was to investigate the effects of ethanol extract of fruit of L. lucidum (ELL) on butylated hydroxytoluene (BHT)-induced oxidative stress in rats. Animals were pre-treated with ELL (250, 500 and 1000 mg/kg/day, orally) for seven days, and then administrated with BHT (1000 mg/kg) by oral. Compared to the BHT (1000 mg/kg)-treated group, results showed that ELL could significantly reduce the levels of serum glutamic pyruvic transaminase (GPT), glutamic oxaloacetic transaminase (GOT), alkaline phosphatase (Alk-P), blood urea nitrogen (BUN), creatinine (Cr), lactate dehydrogenase (LDH) and triglyceride (TG), as well as LDH in BALF. It also significantly decreased the level of lipid peroxidation in liver and lung. In addition, ELL also significantly enhanced the levels of catalase, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in liver, kidney and lung tissues in rats when compared with the BHT-induced group (P < 0.05). Finally, the histopathological evaluation of the tissues revealed that ELL reduced the incidence of lung lesions. According to the results, the protective effect of ELL against acute BHT-induced oxidative stress in rats could be through its antioxidative activities and the upregulation of antioxidative enzymes.
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Lin, Da jun, and 林大鈞. "Protective effects of glucosamine on oxidative-stress injury of retina via modulation of protein O-GlcNAC glycosylation." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/34081446790594344429.
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碩士<br>國防醫學院<br>航太及海底醫學研究所<br>101<br>The report of World Health Organization in 2010 indicated that Glaucoma is one of the main causes of blindness.Glaucoma is a kind of neurodegenerative disease.Excessive intraocular pressure (IOP) caused most of glaucoma. IOP will make the retinal blood vessels are oppressed, retinal ischemia and oxidative stress overload which eventually making the retina ganglion cell apoptosis.Glucosamine(GlcN) is an endogenous amino sugar which has the ability to transfer N-acetylglucosamine(GlcNAc) to serine and threonine residues. This is a protein posttranslational glycosylation. Serine and threonine are also activation domain of protein phosphorylation.If oxidative stress signaling pathways have proteins which can be phosphorylated and glycosylated modification at the same time, glucosamine will increase glycosylated protein to reduce the level of phosphorylation and achieve the purpose of inhibiting apoptosis signals. The results of this experiment show that glucosamine not only have antioxidative property, but also downregulate pP38/ P38 level of MAPK pathway. Therefore, glucosamine can protect retinal ganglion cells from oxidative injury.
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Chen, Yun-Ju, and 陳韻如. "Protective effects of nano/submicron lycium barbarum fruits against oxidative stress – induced diabetic retinopathy in animal models." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/21033117574899322538.
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碩士<br>國立臺灣大學<br>臨床醫學研究所<br>100<br>Diabetes mellitus (DM) is an important disease not only because of its high prevalence but also the disabling systemic complications. In eyes, DM can cause microvascular complication, called diabetic retinopathy (DR). It is a major cause of vision loss in young adults in the developing world and therefore a critical public health issue. Multiple biochemical abnormalities have been documented to be responsible for the pathogenesis of diabetic retinopathy. However, no single event predominates. Among the various pathways and effector molecules, oxidative stress plays a crucial role. Hyperglycemia in DM patients can induce ROS (Reactive oxygen species) production, which stimulates downstream inflammatory mediators and finally causes retinal capillary cells apoptosis. These inflammation-related chemokines and cell adhesion molecules are proved to be related to DR.
Lycium barbarum (LB) fruits, a kind of medicinal plant used in East Asia for over 2300 years, have been studied to posses anti-aging, antioxidant and neuroprotective effects. The active biological activity of LB fruits comes from LBP (Lycium barbarum polysaccharide), zeaxanthin and other small molecules. Some studied showed its antioxidant capacity in various animal models with oxidative stress induced in skin, muscle and liver. However, its protective effect on eyes or retinal tissues has not been fully elucidated.
Therefore, in our study, we investigated if LB fruits had protective effects on DR via antioxidation and anti-inflammation properties. Besides, we also applied nano-technique to prepare LB fruits and assumed this would increase its bioavailability.
In this study, we successfully established a diabetic animal model by intraperitoneal injection of STZ. The result proved that treatment with LB fruits for 60 days could reduce systemic total cholesterol, triglyceride and free radicals as well as urine sugar. In eyes, free radicals and some inflammatory markers including ICAM-1, MCP-1, RANTES, IL-8 and iNOS expressions in aqueous humor and retinas also decreased after treatment of LB fruits. Expression of three oxidative stress responders：HO-1, Prx-1 and TRX also attenuated, reflecting suppressed oxidative stress. In histological changes, retinal sections showed less staining for acrolein, nitrotyrosin and 8-OHdG after LB fruits treatment, indicating inhibited oxidative damages on lipid, protein and DNA.
Milled LB fruits had better protection over blended ones in some aspects, bot not all of the tested markers. So the superior effects of LB fruits after nanotechnology -processing may need further investigations.
Our study concluded that LB fruits had antioxidation and anti-inflammation effects in eyes, in diabetic animal models. The milled LB fruits may have enhanced protection over blended ones. Therefore, LB fruits may serve as an alternative or supplementary treatment in diabetic retinopathy.
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"The Protective Effect of Community Organization on Distress in Disadvantaged Neighborhoods: Considering the Latino Experience in Chicago." Doctoral diss., 2014. http://hdl.handle.net/2286/R.I.24974.
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abstract: Psychological distress occurs at disproportionate rates among minority groups and individuals with lower socioeconomic status. This dissertation focuses on the relationship between living in a disadvantaged neighborhood and distress among Latinos, the formal and informal organizations that mediate the direct and indirect relationship between disadvantage and distress in this population, and the differences of social stress processes based on aspects of Latino social status, linguistic acculturation status, and the percentage of residents in the neighborhood that identify as Latino. This dissertation focuses its investigation on Latinos living in Chicago, specifically asking: In a metropolitan city, can the presence of formal and informal community organizations protect Latinos living in disadvantage neighborhoods from experiencing psychological distress? The findings demonstrate an indirect association between disadvantage and distress though objective disorganization and perception of disorganization. Both the density of community centers and block watch had an indirect protective effect, mediating the relationship between neighborhood disadvantage and distress, but did not decrease the indirect effect of disadvantage on distress through objective or perceptions of disorganization. The results of this dissertation suggest that changes to a neighborhood's environment may decrease population rates of distress in disadvantaged neighborhoods.<br>Dissertation/Thesis<br>Ph.D. Social Work 2014
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Li, Mong-Han, and 李孟翰. "The Protective Effects and Underlying Mechanisms of a New Synthetic Derivative of Caffeic Acid on Cardiomyocytes under Oxidative Stress." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/64679419789611152911.
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碩士<br>國立臺灣大學<br>藥理學研究所<br>102<br>Background: Ischemic heart disease is one of the most prevalent cardiovascular problems in the world. Once ischemia occurs, restoration of blood flow as soon as possible is necessary for minimizing the damage to the least. However, reperfusion injury may even lead to more horrible outcome to the heart. As far, there is still no guideline for treatment of reperfusion injury. Caffeic acid is recognized as a good antioxidant and proved beneficial for cardioprotection by previous works. In this study, we try to figure out whether a synthetic caffeic acid derivative, compound 36-12, has cardioprotective effects under oxidative stress, and investigate the underlying mechanisms as well.
Methods and Results: In this study, 50 μM H2O2 was used to induce oxidative stress in H9c2 cell line to mimic myocardial reperfusion injury. Firstly, we examined the protective effect of compound 36-12 by MTT assay, and compared it with NAC, a well-known antioxidant. Secondly, we measured intracellular ROS level by fluorescent probes to observe antioxidant activity of the drug. Besides, we also used different protein inhibitors to block signaling pathways which make contribution to cardioprotection, and then observed whether the protective effects of compound 36-12 was influenced by doing so. Lastly, activation extents of these proteins at different time points under oxidative stress were shown by Western blotting. Results showed that 3 μM compound 36-12 not only enhanced cell viability but also reduced intracellular ROS level under oxidative stress significantly. This protective effect was comparable to 50 μM NAC. Then, we found that the protective effect of compound 36-12 was totally abolished by STAT3 inhibition, and its ROS scavenging activity was attenuated as well. On the other hand, JAK2 inhibition could enhance cell viability and lower intracellular ROS level under oxidative stress. The results by Western blotting showed that compound 36-12 provoked STAT3 and AMPK phosphorylation obviously. At the same time, however, it also diminished the phosphorylation extent of ERK, as well as H2O2-induced phosphorylation of eNOS and JAK2.
Conclusion: Compound 36-12 shows marvelously cardioprotective and ROS scavenging effects under oxidative stress, which have something to do with activation of STAT3 and inhibition of JAK2. Besides, the phosphorylation of STAT3 induced by compound 36-12, is through a JAK2-independent mechanism.
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Chao, Pei-Yu, and 趙佩玉. "Protective effects of Ocimum gratissimum aqueous extract on the oxidative stress-induced cell apoptosis in Schwann cells and cardiomyoblast cells." Thesis, 2017. http://ndltd.ncl.edu.tw/handle/9rwgc3.
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