Добірка наукової літератури з теми "Medicinsk vit olja"
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Статті в журналах з теми "Medicinsk vit olja":
1
Dell'Agli, Mario, Omar Maschi, Germana V. Galli, Rossana Fagnani, Esther Dal Cero, Donatella Caruso, and Enrica Bosisio. "Inhibition of platelet aggregation by olive oil phenols via cAMP-phosphodiesterase." British Journal of Nutrition 99, no. 5 (May 2008): 945–51. http://dx.doi.org/10.1017/s0007114507837470.
Анотація:
The aim of the present study was to confirm that olive oil phenols reduce human platelet aggregability and to verify the hypothesis that cAMP- and cGMP- phosphodiesterases (PDE) could be one of the targets of the biological effect. Four extracts from oils characterized by a high phenol content (HPE), and low phenol levels (LPE) were prepared and analyzed quali- and quantitatively by HPLC-UV and electrospray ionization–MS/MS. Human washed platelets stimulated with thrombin were used for the aggregation assay. Human platelet cAMP-PDE and recombinant PDE5A1 were used as enzyme source. Platelet aggregation and enzyme activity were assayed in the presence of HPE, LPE and individual phenols. The phenol content of HPE ranged between 250 and 500 mg/kg, whereas the LPE content was 46 mg/kg. The compounds identified were hydroxytyrosol (HT), tyrosol (TY), oleuropein aglycone (OleA) and the flavonoids quercetin (QU), luteolin (LU) and apigenin (AP). OleA was the most abundant phenol (range 23·3 to 37·7 %) and LU was the most abundant flavonoid in the extracts. Oil extracts inhibited platelet aggregation with an 50% inhibitory concentration interval of 1·23–11·2 μg/ml. The inhibitory effect of individual compounds (10 μm) including homovanillyl alcohol (HVA) followed this order: OleA>LU>HT = TY = QU = HVA, while AP was inactive. All the extracts inhibited cAMP-PDE, while no significant inhibition of PDE5A1 (50μg/ml) was observed. All the flavonoids and OleA inhibited cAMP-PDE, whereas HT, TY, HVA (100 μm) were inactive. Olive oil extracts and part of its phenolic constituents inhibit platelet aggregation; cAMP-PDE inhibition is one mechanism through which olive oil phenols inhibit platelet aggregation.
2
Li, Daowen, Xingyao Pei, Xiaoling Qin, Xinyu Liu, Cun Li, Liuan Li, Chongshan Dai, Xilong Xiao, and Shusheng Tang. "Olaquindox-Induced Liver Damage Involved the Crosstalk of Oxidative Stress and p53 In Vivo and In Vitro." Oxidative Medicine and Cellular Longevity 2020 (December 18, 2020): 1–18. http://dx.doi.org/10.1155/2020/8835207.
Анотація:
Olaquindox (OLA), a member of the quinoxaline-N,N-dioxide family, has been widely used as a growth-promoting feed additive and treatment for bacterial infections. The toxicity has been a major concern, and the precise molecular mechanism remains poorly understood. The present study was aimed at investigating the roles of oxidative stress and p53 in OLA-caused liver damage. In a mouse model, OLA administration could markedly cause liver injury as well as the induction of oxidative stress and activation of p53. Antioxidant N-acetylcysteine (NAC) inhibited OLA-induced oxidative stress and p53 activation in vivo. Furthermore, knockout of the p53 gene could significantly inhibit OLA-induced liver damage by inhibiting oxidative stress and the mitochondria apoptotic pathway, compared to the p53 wild-type liver tissue. The cell model in vitro further demonstrated that p53 knockout or knockdown in the HCT116 cell and L02 cell significantly inhibited cell apoptosis and increased cell viability, presented by suppressing ROS production, oxidative stress, and the Nrf2/HO-1 pathway. Moreover, loss of p53 decreased OLA-induced mitochondrial dysfunction and caspase activations, with the evidence of inhibited activation of phosphorylation- (p-) p38 and p-JNK and upregulated cell autophagy via activation of the LC3 and Beclin1 pathway in HCT116 and L02 cells. Taken together, our findings provided a support that p53 primarily played a proapoptotic role in OLA-induced liver damage against oxidative stress and mitochondrial dysfunction, which were largely dependent on suppression of the JNK/p38 pathway and upregulation of the autophagy pathway via activation of LC3 and Beclin1.
3
Song, Chaoran, Deok Jeong, Yo Han Hong, Wan Yi Li, Sang Woo Lee, Mohammad Amjad Hossain, Amani Taamalli, Ji Hye Kim, Jong-Hoon Kim та Jae Youl Cho. "Anti-Inflammatory and Photoaging-Protective Effects of Olea europaea through Inhibition of AP-1 and NF-κ B Pathways". American Journal of Chinese Medicine 48, № 08 (січень 2020): 1895–913. http://dx.doi.org/10.1142/s0192415x20500950.
Анотація:
Olea europaea is a beneficial edible plant with a number of biological activities like anti-inflammatory, anti-oxidant, antithrombic, antihyperglycemic, and anti-ischemic activities. The mechanisms behind the antiphotoaging and anti-inflammatory effects of Olea europaea are not fully understood. To investigate how an ethanol extract of Olea europaea (Oe-EE) exerts these effects, we explored its activities in human keratinocytes and dermal fibroblasts. We assessed the anti-oxidant effects of Oe-EE via 2,2-diphenyl-1-picrylhydrazyl (DPPH) and 2,2[Formula: see text]-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt (ABTS) assays and measured the expression levels of matrix metalloproteinases (MMPs), cyclooxygenase-2, interleukin (IL)-6, tumor necrosis factor (TNF)-[Formula: see text], and moisturizing factors. Antiphotoaging and anti-inflammatory mechanisms of Oe-EE were explored by assessing signaling molecule activation via immunoblotting. Oe-EE treatment decreased the mRNA expression level of MMPs, cyclooxygenase-2, IL-6, and TNF-[Formula: see text] and restored type I collagen, filaggrin, and sirtuin 1 expression in UVB-irradiated cells. Furthermore, Oe-EE inhibited the activities of several activator protein 1 regulatory enzymes, including extracellular signal-regulated kinase (ERK), p38, and c-Jun N-terminal kinase (JNK), and inhibited nuclear factor (NF)-[Formula: see text]B pathway signaling proteins. Therefore, our results indicate that Oe-EE has photoaging-protective and anti-inflammatory effects.
4
Aumeeruddy, Muhammad Zakariyyah, and Mohamad Fawzi Mahomoodally. "Ethnomedicinal Plants for the Management of Diabetes Worldwide: A Systematic Review." Current Medicinal Chemistry 28, no. 23 (August 2, 2021): 4670–93. http://dx.doi.org/10.2174/0929867328666210121123037.
Анотація:
Background: The increasing incidence of diabetes worldwide has urged researchers to explore novel antidiabetic agents from natural products. Ethnomedicinal field studies on diabetes have expanded across the globe, documenting large numbers of folk medicinal plants against diabetes. Nonetheless, a systematic review of these surveys has not been conducted so far. This study documents the medicinal plants traditionally used globally for managing diabetes. Methods: Key databases including Sciencedirect, Medline/PubMed, and Google Scholar were scrutinized. The Plant List and The International Plant Names Index (IPNI) were used to validate the scientific plant names. Results: 2004 traditionally used plants belonging to 1112 genera and 197 families were reported across 92 countries for the management of diabetes. Leguminosae (105 genera and 193 species), Compositae (97 genera and 188 species), and Lamiaceae (47 genera and 121 species) were the main plant families reported. Momordica charantia L., Syzygium cumini (L.) Skeels, Allium sativum L., Azadirachta indica A.Juss., Catharanthus roseus (L.) G.Don, Olea europaea L., Trigonella foenum-graecum L., Gymnema sylvestre (Retz.) R.Br. ex Sm., Aloe vera (L.) Burm.f., and Allium cepa L were the species mostly reported. Indeed, the antidiabetic properties of these main species have been evidenced by experimental studies. Several antidiabetic compounds acting via different mechanisms have been identified, including momordicoside, karaviloside, cucurbitacin, charantin, and charantoside from M. charantia, cuminoside from S. cumini, S-allyl cysteine sulfoxide from A. sativum, limonoids from A. indica, alkaloids including vindoline, vindolidine, vindolicine and vindolinine from C. roseus, oleuropein and oleanolic acid from O. europaea, flavone C-glycosides such as vicenin-1, isoschaftoside, and schaftoside from T. foenum-graecum seeds, gymnemosides, gymnemagenin, and pregnane glycosides from G. sylvestre, chysalodin from A. vera, and quercetin from A. cepa. Conclusion: This review is the first to provide a compiled list of traditional medicinal plants used worldwide against diabetes.
5
Bao, Jiapeng, Weifeng Yan, Kai Xu, Mengyao Chen, Zhonggai Chen, Jisheng Ran, Yan Xiong, Lidong Wu та Ratanesh K. Seth. "Oleanolic Acid Decreases IL-1β-Induced Activation of Fibroblast-Like Synoviocytes via the SIRT3-NF-κB Axis in Osteoarthritis". Oxidative Medicine and Cellular Longevity 2020 (28 вересня 2020): 1–10. http://dx.doi.org/10.1155/2020/7517219.
Анотація:
Synovial inflammation is a major pathological feature of osteoarthritis (OA), which is a chronic degenerative joint disease. Fibroblast-like synoviocytes (FLS), localized in the synovial membrane, are specialized secretory cells. During OA synovitis, FLS produce chemokines and cytokines that stimulate chondrocytes to secrete inflammatory cytokines and activate matrix metalloproteinases (MMPs) in FLS. Recent studies have demonstrated that sirtuin 3 (SIRT3) performs as a key regulator in maintaining mitochondrial homeostasis in OA. This study aims at ascertaining whether SIRT3 is involved in OA synovitis. The overexpression (OE) and knockdown (KD) of SIRT3 are established by short hairpin RNA (shRNA) and recombinant plasmid in human FLS. The anti-inflammatory effect of SIRT3 underlying in oleanolic acid- (OLA-) prevented interleukin-1β- (IL-1β-) induced FLS dysfunction is then evaluated in vitro. Additionally, the molecular mechanisms of SIRT3 are assessed, and the interaction between SIRT3 and NF-κB is investigated. The data suggested that SIRT3 can be detected in human synovial tissues during OA, and OLA could elevate SIRT3 expression. OE-SIRT3 and OLA exhibited equal authenticity to repress inflammation and reverse oxidative stress changes in IL-1β-induced human FLS dysfunction. KD-SIRT3 was found to exacerbate inflammation and oxidative stress changes in human FLS. Furthermore, it was found that SIRT3 could directly bind with NF-κB, resulting in the suppression of NF-κB activation induced by IL-1β in human FLS, which then repressed synovial inflammation in OA. In general, the activation of SIRT3 by OLA inhibited synovial inflammation by suppressing the NF-κB signal pathway in FLS, and this suggested that SIRT3 is a potential target for OA synovitis therapy.
6
El-Hamoly, Tarek, Zoltán Hajnády, Máté Nagy-Pénzes, Edina Bakondi, Zsolt Regdon, Máté A. Demény, Katalin Kovács, et al. "Poly(ADP-Ribose) Polymerase 1 Promotes Inflammation and Fibrosis in a Mouse Model of Chronic Pancreatitis." International Journal of Molecular Sciences 22, no. 7 (March 30, 2021): 3593. http://dx.doi.org/10.3390/ijms22073593.
Анотація:
Chronic pancreatitis (CP) is an inflammatory disease of the pancreas characterized by ductal obstructions, tissue fibrosis, atrophy and exocrine and endocrine pancreatic insufficiency. However, our understanding is very limited concerning the disease’s progression from a single acute inflammation, via recurrent acute pancreatitis (AP) and early CP, to the late stage CP. Poly(ADP-ribose) polymerase 1 (PARP1) is a DNA damage sensor enzyme activated mostly by oxidative DNA damage. As a co-activator of inflammatory transcription factors, PARP1 is a central mediator of the inflammatory response and it has also been implicated in acute pancreatitis. Here, we set out to investigate whether PARP1 contributed to the pathogenesis of CP. We found that the clinically used PARP inhibitor olaparib (OLA) had protective effects in a murine model of CP induced by multiple cerulein injections. OLA reduced pancreas atrophy and expression of the inflammatory mediators TNFα and interleukin-6 (IL-6), both in the pancreas and in the lungs. Moreover, there was significantly less fibrosis (Masson’s trichrome staining) in the pancreatic sections of OLA-treated mice compared to the cerulein-only group. mRNA expression of the fibrosis markers TGFβ, smooth muscle actin (SMA), and collagen-1 were markedly reduced by OLA. CP was also induced in PARP1 knockout (KO) mice and their wild-type (WT) counterparts. Inflammation and fibrosis markers showed lower expression in the KO compared to the WT mice. Moreover, reduced granulocyte infiltration (tissue myeloperoxidase activity) and a lower elevation of serum amylase and lipase activity could also be detected in the KO mice. Furthermore, primary acinar cells isolated from KO mice were also protected from cerulein-induced toxicity compared to WT cells. In summary, our data suggest that PARP inhibitors may be promising candidates for repurposing to treat not only acute but chronic pancreatitis as well.
7
Tezcan, G., SA Aksoy, B. Tunca, A. Bekar, M. Mutlu, G. Cecener, U. Egeli, H. Kocaeli, H. Demirci, and MO Taskapilioglu. "Oleuropein modulates glioblastoma miRNA pattern different from Olea europaea leaf extract." Human & Experimental Toxicology 38, no. 9 (June 6, 2019): 1102–10. http://dx.doi.org/10.1177/0960327119855123.
Анотація:
Glioblastoma (GBM) is the most prevalent and deadliest subtype of glioma. Despite current innovations in existing therapeutic modalities, GBM remains incurable, and alternative therapies are required. Previously, we demonstrated that Olea europaea leaf extract (OLE) kills GBM cells by modulating miR-181b, miR-137, miR-153 and Let-7d expression. However, although oleuropein (OL) is the main compound in OLE, its role in the antitumour effect of OLE remains unknown. This study determined the effect of OL on GBM cell line T98G and compared the results with our previous findings regarding the effect of OLE on the same cell line. The antiproliferative activity of OL and its effect on temozolomide (TMZ) response were tested inT98G cells using WST-1 assay. OL inhibition was evaluated using one-way analysis of variance with Tukey’s post hoc test. The effect of OL on miR-181b, miR-137, miR-153 and Let-7d expression was assessed using quantitative reverse transcription polymerase chain reaction. Fold differences in expression between untreated, OL or OL + TMZ-treated samples were calculated using 2−ΔCt method. Significance was evaluated using an independent sample t-test. Treatment with 277.5 and 555 µM OL resulted in 39.51% and 75.40% reductions in T98G cells within 24 h. Coadministration of 325 µM TMZ and 277.5 or 555 µM, OL caused 2.08- and 2.83-fold increases, respectively, in the therapeutic effect of TMZ. OL + TMZ significantly increased microRNA expression, particularly Let-7d, than OLE. In conclusion, OL has an antitumour effect on GBM cells mainly via regulation of Let-7d expression. The present results also indicate other minor compounds in OLE play important anticancer roles.
8
Misra, Ranjita, Bamadeb Patra, Sudha Varadharaj, and Rama Shanker Verma. "Establishing the promising role of novel combination of triple therapeutics delivery using polymeric nanoparticles for Triple negative breast cancer therapy." BioImpacts 11, no. 3 (July 31, 2020): 199–207. http://dx.doi.org/10.34172/bi.2021.27.
Анотація:
Introduction: Triple-negative breast cancer (TNBC) is a lethal tumor with an advanced degree of metastasis and poor survivability as compared to other subtypes of breast cancer. TNBC which consists of 15 % of all types of breast cancer is categorized by the absence of expression of estrogen receptors (ER), progesterone receptors (PR) and human epidermal growth factor receptor-2 (HER2). This is the main reason for the failure of current hormonal receptor-based therapies against TNBCs, thus leading to poor patient outcomes. Therefore, there is a necessity to develop novel therapies targeting this devastating disease. Methods: In this study, we have targeted TNBC by simultaneous activation of apoptosis through DNA damage via cytotoxic agent such as paclitaxel (PAC), inhibition of PARP activity via PARP inhibitor, olaparib (OLA) and inhibiting the activity of FOXM1 proto-oncogenic transcription factor by using RNA interference technology (FOXM1-siRNA) in nanoformulations. Experiments conducted in this investigation include cellular uptake, cytotoxicity and apoptosis study using MDA-MB-231 cells. Results: The present study validates that co-delivery of two drugs (PAC and OLA) along with FOXM1-siRNA by cationic NPs, enhances the therapeutic outcome leading to greater cytotoxicity in TNBC cells. Conclusion: The current investigation focuses on designing a multifunctional drug delivery platform for concurrent delivery of either PAC or PARP inhibitor (olaparib) and FOXM1 siRNA in chitosan-coated poly(D, L-lactide-co-glycolide) (PLGA) nanoparticles (NPs) with the ability to emerge as a front runner therapeutic for TNBC therapy.
9
Qiu, Mingning, Jie Liu, Yongxia Su, Rong Guo, Baoyu Zhao, and Jianjun Liu. "Diosmetin Induces Apoptosis by Downregulating AKT Phosphorylation via P53 Activation in Human Renal Carcinoma ACHN Cells." Protein & Peptide Letters 27, no. 10 (November 2, 2020): 1022–28. http://dx.doi.org/10.2174/0929866527666200330172646.
Анотація:
Background: Diosmetin (DIOS) is the aglycone of the flavonoid glycoside, diosmin, derived naturally from the leaves of the legume, Olea europaea, and Acacia farnesiana. It has potent anticancer activity against multiple forms of cancers. However, the role of DIOS in renal carcinoma and its mechanism of action remain unclear. Objective: The purpose of this study is to investigate the effect of DIOS on cell viability and apoptosis in renal carcinoma cells and explore the possible mechanism of action. Methods: Cell viability, cytotoxicity, caspase activity, apoptosis, and expression of apoptotic related proteins were analyzed in renal carcinoma ACHN cells. Results: The results showed that DIOS inhibited the cell viability, and induced cytotoxicity and apoptosis in ACHN cells. Furthermore, DIOS increased expression of p53 mRNA and proteins, and downregulated phosphorylation of the phosphoinositide 3-kinase and protein B kinase (PI3K/AKT). In addition, it was observed that the anticancer effect of DIOS was significantly enhanced by the p53 activator, but inhibited by the p53 inhibitor. Conclusion: Our data suggested that DIOS induced apoptosis in renal carcinoma ACHN cells by reducing AKT phosphorylation through p53 upregulation.
10
De la Ossa, Felice, Azimi, Salsano, Digiacomo, Macchia, Danti, and Di Stefano. "Waste Autochthonous Tuscan Olive Leaves (Olea europaea var. Olivastra seggianese) as Antioxidant Source for Biomedicine." International Journal of Molecular Sciences 20, no. 23 (November 25, 2019): 5918. http://dx.doi.org/10.3390/ijms20235918.
Анотація:
Olive leaf extract (OLE) can be obtained as biowaste and is extensively used a food supplement and an over-the-counter drug for its beneficial effects. New studies have investigated OLE concerning the role of oxidative stress in the pathogenesis of vascular disease. This in vitro study aims to evaluate if OLE extracted from the Tuscan Olea europaea protects endothelial cells against oxidative stress generated by reactive oxygen species (ROS). Methods: OLE total polyphenols (TPs) were characterized by the Folin–Ciocalteu method. Endothelial cells were grown in conventional cultures (i.e., two-dimensional, 2D) and on a biomaterial scaffold (i.e., three-dimensional, 3D) fabricated via electrospinning. Cell viability and ROS measurement after H2O2 insults were performed. Results: OLE TP content was 23.29 mg GAE/g, and oleuropein was the principal compound. The dose-dependent viability curve highlighted the absence of significant cytotoxic effects at OLE concentrations below 250 µg/mL TPs. By using OLE preconditioning at 100 µg/mL, cell viability decrease was observed, being in 3D lower than in the 2D model. OLE was protective against ROS in both models. Conclusions: OLE represents a high-value antioxidant source obtained by biowaste that is interesting for biomedical products. Using a 3D scaffold could be the best predictive model to mimic the physiological conditions of vascular tissue reaction.
Дисертації з теми "Medicinsk vit olja":
1
Dubeck, Schömer Hanna. "Medical White Oil in Cosmetic Applications." Thesis, KTH, Kemi, 2021. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-301785.
Анотація:
Fuktbevarare är de produkter som oftast skrivs och rekommenderas av dermatologer, och den vanligaste typen av fuktgivare är lotioner och krämer. Dessa produkter är emulsioner, vilka ofta innehåller medicinsk vit olja (MWO) på grund av deras skyddande egenskaper samt enastående hudkompabilitet. Traditionellt så har de MWO som används varit parafinska. Då naftenoljor ofta har visat sig ha bättre emulsions stabilitet, har detta examensarbete ämnat attjämföra emulsions stabiliteten för Nynas ABs nya MWO, N-MWO, med en parafinsk motsvarighet, P-MWO. Jämförelsen av de två oljorna genomfördes genom att variera följande faktorer: olje- och emulgator typ, koncentration av emulgator samt både med och utan parfym. De två emulgator system som användes bestod av Promulgen D (en kommersiell produkt från Lubrizol) samt kombinationen av Tween 80 och Span 20. Bättre emulsionsstabilitet och mindre droppstorlek och fördelning utficks då högre koncentration Promulgen D användes. En högre koncentration av Tween 80 och Span 20 gav dock inte samma gynnsamma effekt. Resultaten från samtliga tester påvisade att emulsions stabiliteten inte påverkades utav parfym. Det som istället gav störst påverkan var typ av emulgator. De prover som innehöll P-MWO samt Tween 80 och Span 20 fasseparerade. Detta berodde dock troligen mer på att P-MWO inte var kompatibel med dessa emulgatorer eftersom oljetypen inte påverkade emulsionsstabiliteten när Promulgen D användes som emulgator.Moisturizers are the most prescribed products in dermatology, and the most common type of moisturizer delivery systems are lotions and creams. These are emulsions and often contain medical white oil (MWO) due to their protective properties and excellent skin compatibility. The MWO used in cosmetics have traditionally been paraffinic. However, as naphthenic oils often have been proven to create better emulsion stability, this thesis aimed to compare Nynas AB's new MWO, N-MWO, with a paraffinic oil, P-MWO, with similar properties regarding their emulsion stability. The two oils were compared by analyzing their emulsion stability using a rheometer and a Mastersizer 3000 while varying the following factors: type of oil, type of emulsifier, emulsifier concentration, and with and without perfume. The two emulsifying systems used were the commercial product Promulgen D from Lubrizol and the combination of Tween 80 and Span 20. Better emulsion stability and smaller droplet size distribution were obtained when a higher content of Promulgen D was added. However, a higher concentration of Tween 80 and Span 20 did not have the same favorable effect. The results showed that the addition of perfume had no effect, while the type of emulsifier influenced the emulsion stability the most. The samples made from Supela 240 and Tween 80 and Span 20 phase separated. This was more likely due to P-MWOs incompatibility with these emulsifiers as oil type did not influence the emulsion stability when Promulgen D was used as an emulsifier.