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Academic literature on the topic 'HT-22 cell line'
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Journal articles on the topic "HT-22 cell line"
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Qi, Huizhen, та Liang Liu. "Rhoifolin attenuates damage to hippocampal neuronal culture model of acquired epilepsy in vitro by regulating NF-κB/iNOS/COX-2 axis". Quality Assurance and Safety of Crops & Foods 14, № 3 (2022): 116–23. http://dx.doi.org/10.15586/qas.v14i3.1093.
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To assess the effect of Rhoifolin (ROF [apigenin 7-O-enneohesperidoside]) on the damage to hippocampal neu-ronal culture model of acquired epilepsy (AE) and investigate its possible mechanisms. A hippocampal neuronal culture model of AE was established through incubating HT-22 cells with MgCl2 free medium. 3-(4,5-Dimethylth-iazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assays were used to assess the effect of ROF on cell viability and apoptosis exposed to epilepsy. The oxidative stress and secretion of inflammatory cytokines were measured by reverse transcription-quantitative polymerase chain reaction and enzyme-linked-immunosorbent serologic assay, respectively. Immunoblot assays were performed to determine the protein expression levels of nuclear factor kappa B/nitric oxide synthases/cyclooxygenase-2 (NF-κB/iNOS/COX-2) axis. ROF increases viability and reduces apoptosis of AE medium-treated HT-22 cell line. ROF relieves oxidative stress in AE medium-treated HT-22 cell line. ROF decreases the levels of pro-inflammatory cytokines in AE medium-treated HT-22 cell line. The functional effects of ROF on AE medium-treated HT-22 cell line is through inhibiting NF-κB/iNOS/COX-2 axis. ROF increased viability, decreased apoptosis, suppressed oxidative stress, and reduced pro-inflammatory cytokine levels in an epilepsy model in vitro by inhibiting NF-κB/iNOS/COX-2 axis. ROF might serve as a potential drug for epilepsy treatment.
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Kim, Si-Yeon, Jung-Ho Lee, and Soon-Ae Kim. "Zinc Deficiency Induces Autophagy in HT-22 Mouse Hippocampal Neuronal Cell Line." International Journal of Molecular Sciences 23, no. 15 (2022): 8811. http://dx.doi.org/10.3390/ijms23158811.
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Zinc is a trace metal vital for various functions in nerve cells, although the effect of zinc deficiency on neuronal autophagy remains unclear. This study aimed to elucidate whether zinc deficiency induced by treatment with N, N, N′, N′-tetrakis (2-pyridylmethyl) ethylenediamine (TPEN), a zinc chelator, affects and alters autophagy activity. In cell viability assays, TPEN showed cytotoxicity in HT-22 cells. TPEN treatment also increased LC3-II levels and the ratio of LC3-II to LC3-I. Western blot analysis showed that phospho-AMP-activated protein kinase levels and the ratio of phospho-AMP-activated protein kinase to total AMP-activated protein kinase increased. Protein levels of the mammalian target of rapamycin and sirtuin 1 decreased following TPEN treatment. When TPEN-treated HT-22 cells were cotreated with autophagy inhibitors, 3-methyladenine (1 mM), or bafilomycin A1 (3 nM), the TPEN-induced decrease in cell viability was exacerbated. Cotreatment with chloroquine (10 μM) partially restored cell viability. The study showed that zinc deficiency induces autophagy and may be cytoprotective in neurons. We expect our results to add a new perspective to our understanding of the neuronal pathology related to zinc deficiency.
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V., Karri, Kumar V., Ramos D., Oliveira E., and Schuhmacher M. "An in vitro cytotoxic approach to assess the toxicity of heavy metals and their binary mixtures on hippocampal HT-22 cell line." Toxicology letters 282 (October 5, 2017): 25–36. https://doi.org/10.1016/j.toxlet.2017.10.002.
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Humans are exposed to a cocktail of heavy metal toxicants in the environment. Though heavy metals are deleterious, there is a paucity of information on the toxicity of mixtures. In this study, four common neurotoxicity heavy metals lead (Pb) cadmium (Cd), arsenic (As), and methylmercury (MeHg) were exposed individually and as mixtures to HT-22 cell line for 8days. The study established that low dose exposures induced toxicity to the HT-22 cell line during 8days. The results indicates potency dependent response, the toxicity of single metals on the HT-22 cells; MeHg > As > Cd > Pb. The cytotoxicity data of single metals were used to determine the mixtures interaction profile by using the dose additivity and effect additivity method. Metal mixtures showed higher toxicities compared to individual metals. Synergistic, antagonistic or additive effects of the toxicity were observed in different mixtures in low dose exposure. The interactive responses of mixtures depend on the co-exposure metal and their respective concentration. We concluded that the combined effects should be considered in the risk assessment of heavy metal co-exposure and potency. In future, comprehensive mechanistic based investigations needed for understanding the real interactive mixtures effects at molecular level.
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Sandberg, Maxwell, Wyatt Whitman, Christina Ross, Matvey Tsivian, and Stephen Walker. "Pulsed electromagnetic field therapy's effect on bladder cancer cell line HT-1376." Journal of Clinical Oncology 42, no. 4_suppl (2024): 666. http://dx.doi.org/10.1200/jco.2024.42.4_suppl.666.
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666 Background: Pulsed electromagnetic field therapy (PEMF) is a magnetic waveform energy that can be targeted for delivery to cells and/or patients. It is noninvasive, and to date no reported negative side effects exist. Recently, its use as a therapeutic for cancer has come into focus. However, to our knowledge, no study has examined the effect of PEMF on bladder cancer at the cellular level. In this study, we sought to examine how PEMF altered a bladder cancer cell line (HT-1376) at the genomic level. Methods: HT-1376 cells were cultured, and cells were plated into either a control plate (no PEMF) or experimental plate (PEMF). The experimental cells were subjected to PEMF which had an oscillating magnetic field ranging from 1.5 MilliTesla (mT) to 16 mT at 30 Hertz, 1 hour each day for 3 total days. RNA was isolated from both control and experimental cell plates on day 3 and assayed on whole genome microarrays. Day 3 control samples from HT-1376 were compared to day 3 PEMF treated cells. Results were analyzed using Ingenuity Pathway Analysis. Results: Data from genomic analysis revealed that many cancer-related pathways were altered after treatment with PEMF in HT-1376. Relevant cancer pathways downregulated after PEMF treatment in HT-1376 cells compared to controls were the PIK3/AKT pathway (p=8.1e-61), neuroinflammation signaling pathway (p=2.3e-60), and external growth factor pathway (p=4.8e-35). Upregulated pathways after PEMF treatment relative to controls were the p53 signaling pathway (p=1.1e-06), endocannabinoid cancer inhibition pathway (p=1.1e-38), and the T-cell exhaustion signaling pathway (p=3.7e-22). The table also lists cancer relevant genes up and downregulated after PEMF treatment. Conclusions: PEMF appears to alter the tumor profile of bladder cancer cell line HT-1376. Key pathways implicated in cancer pathogenesis were altered after treatment. Further, after treating HT-1376 bladder cancer cells with PEMF for 3 days, significant alterations in gene expression occurred. This has widespread implications for prognosis, management, and treatment of bladder cancer. Ultimately, PEMF may represent an exciting new non-invasive therapeutic in bladder cancer, which necessitates further research.[Table: see text]
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Soylu, Sinan. "Crocus Officinalis (L.) Extract on Human Colerectal Cancer Cell Line (HT-22): Investigation in Vitro." Cumhuriyet Science Journal 45, no. 1 (2024): 35–39. http://dx.doi.org/10.17776/csj.1419826.
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Crocus sativus L. has been used as spice, food colouring and medicinal plant for thousands of years. In this study, antioxidant properties and cytotoxic effect of saffron extract were evaluated in HT-22 cell lines. Malignant and non-malignant cells (L929) were cultured in DMEM medium and incubated with different concentrations of saffron extract in different solvents (water, ethanol, ethyl-acetate, n-hexane). Cell viability was determined by MTT assay. Antioxidant parameters such as DPPH, FRAP, total polyphenol and flavonoid amounts were measured. The highest DPPH value was found as 15.90±0.12 µg/mL in ethyl acetate solvent. Total polyphenols were 89.06±0.02 mg GAE/g extract, flavonoids were 76.98±2.08 µg QE/g extract and FRAP was 67.93±0.98 mg/g extract in ethanol solvent. In colon cancer, IC50 value 94±1.37 µg/mL was found to be the highest value. This is thought to be due to the high antioxidant capacity in ethanol solvent. While antioxidant capacity was not found to be high, antiproliferation effect was found to be high. Saffron may also be considered as a promising chemotherapeutic agent in cancer treatment in the future.
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Karri, Venkatanaidu, Marta Schuhmacher, Vikas Kumar, David Ramos, and Eliandre De Oliveira Cacheado. "Proteomics approach for improving the mechanisms associated with MeHg toxicity in HT-22 hippocampal cell line." Toxicology Letters 280 (October 2017): S259. http://dx.doi.org/10.1016/j.toxlet.2017.07.920.
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Ji, Yang‐Fei, Dan Wang, Yan‐Ru Liu, Xing‐Rong Ma, Hong Lu, and Bo‐Ai Zhang. "MicroRNA‐132 attenuates LPS‐induced inflammatory injury by targeting TRAF6 in neuronal cell line HT‐22." Journal of Cellular Biochemistry 119, no. 7 (2018): 5528–37. http://dx.doi.org/10.1002/jcb.26720.
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Illmer, Christoph, Sibylle Madlener, Zsuzsanna Horvath, et al. "Immunologic and Biochemical Effects of the Fermented Wheat Germ Extract Avemar." Experimental Biology and Medicine 230, no. 2 (2005): 144–49. http://dx.doi.org/10.1177/153537020523000209.
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Avemar (MSC) is a nontoxic fermented wheat germ extract demonstrated to have antitumor effects. Avemar has the potential to significantly improve the survival rate in patients suffering from malignant colon tumors. We studied its effects in the HT-29 human colon carcinoma cell line. Avemar had an inhibiting effect on colonies of HT-29 cells with an IC50 value of 118 μg/ml (7 days of incubation); this value could be decreased to 100 and 75 μg/ml in the presence of vitamin C. In the cell line examined, Avemar induced both necrosis and apoptosis, as demonstrated by Hoechst/propldium iodide staining. The incubation of cells with 3200 μg/ml Avemar for 24 hrs caused necrosis in 28% and the induction of apoptosis in 22% of the cells. Avemar inhibited the cell-cycle progression of HT-29 cells in the G1 phase of the cell cycle. In addition, Avemar inhibited the activity of the key enzyme of de novo DNA synthesis, ribonucleotide reductase. In addition, we determined the effects of Avemar on the activity of cyclooxygenase-1 and -2. Both enzymes were significantly inhibited by Avemar with IC50 values of 100 and 300 μg/ml, respectively. We outline new explanations for its antitumor activity, which might serve as the basis for further studies using Avemar.
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Rae, Julie, Jason Hackney, Kevin Huang, Mary Keir, and Ann Herman. "Identification of an IL-22-Dependent Gene Signature as a Pharmacodynamic Biomarker." International Journal of Molecular Sciences 22, no. 15 (2021): 8205. http://dx.doi.org/10.3390/ijms22158205.
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Interleukin-22 (IL-22) plays a role in epithelial barrier function and repair, and may provide benefits in conditions like inflammatory bowel disease. However, limited human data are available to assess the clinical effect of IL-22 administration. This study used a human intestinal cell line to identify an IL-22-dependent gene signature that could serve as a pharmacodynamic biomarker for IL-22 therapy. The response to IL-22Fc (UTTR1147A, an Fc-stabilized version of IL-22) was assessed in HT-29 cells by microarray, and the selected responsive genes were confirmed by qPCR. HT-29 cells demonstrated dose-dependent increases in STAT3 phosphorylation and multiple gene expression changes in response to UTTR1147A. Genes were selected that were upregulated by UTTR1147A, but to a lesser extent by IL-6, which also signals via STAT3. IL-1R1 was highly upregulated by UTTR1147A, and differential gene expression patterns were observed in response to IL-22Fc in the presence of IL-1β. An IL-22-dependent gene signature was identified that could serve as a pharmacodynamic biomarker in intestinal biopsies to support the clinical development of an IL-22 therapeutic. The differential gene expression pattern in the presence of IL-1β suggests that an inflammatory cytokine milieu in the disease setting could influence the clinical responses to IL-22.
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Betul, Danısman, and Cicek Betul. "Agomelatine protects hippocampal neurons against doxorubicin induced toxicity." GSC Biological and Pharmaceutical Sciences 24, no. 2 (2023): 290–96. https://doi.org/10.5281/zenodo.10440942.
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Doxorubicin (DOX) is a powerful chemotherapy drug used in numerous cancer treatments, known to causes neurotoxicity and impair cognitive function in cancer patients. The main mechanism thought to be responsible for the neuronal damage related to chemotherapy is oxidative stress. Agomelatine (AGM) has recently been identified as a neuroprotective agent against toxicity and the effect of AGM on DOX-induced neurotoxicity was investigated in this study. In order to evaluate the effect of AGM on oxidative stress and apoptosis, malondialdehyde (MDA), lactate dehydrogenase (LDH), superoxide dismutase (SOD), catalase (CAT), and Caspase-3 expression were analyzed in the HT-22 cell line. AGM considerably reduced oxidative damage due to DOX in vitro. MDA and Caspase-3 were considerably higher in the DOX group. These values were dramatically decreased by AGM. AGM greatly increased the CAT and SOD levels when compared to the DOX group. These results suggest that DOX therapy alters antioxidant status in hippocampus, a critical cognition-related region. So if we are aware of the functional effects of DOX, it is possible to avoid some of the disabling side effects of chemotherapy in cancer patients and may prevent these effects with antioxidant agents such as AGM
Dissertations / Theses on the topic "HT-22 cell line"
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Karri, Venkatanaidu. "Integrated In vitro - Omics based Approach to assess the Heavy metals and their Binary mixtures toxicity in Hippocampal HT-22 cell line." Doctoral thesis, Universitat Rovira i Virgili, 2018. http://hdl.handle.net/10803/553243.
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Els estudis toxicol'ogics d'avui dia fan l'avaluació d'exposicions i riscos en el cervell sense abordar adequadament les
possibles interaccions de metalls en la regió del cervell de l'hipocamp. Es va avaluar la neurotoxicitat similar / disímil
de cada metall en el cervell que pot donar un fort suport a l'efecte de mescles en el cervell (Capítol 1). L'abast del
nostre estudi és provar el metall únic (Pb, Cd, As i MeHg) i les seves mescles d'impacte tòxic crònic en la línia
cel·lular hipocamp HT-22 mitjançant l'ús de la metodologia de biologia in vitro i del sistema. Inicialment, es van
realitzar assaigs de citotoxicitat, apoptosi i genotoxicitat de metalls simples per avaluar la potència tòxica de cada
metall, el perfil d'interacció de les mescles en cèl·lules hipocampals (capítol 2, 3). Els resultats obtinguts mostren
clarament la potència dels metalls MeHg> As> Cd> Pb. Un altre objectiu de l'estudi (capítol 4) va ser la toxicitat dels
metalls pesants en cèl·lules HT-22 utilitzant (Pb, Cd, As i MeHg), ja que algunes proteïnes d'estrès podrien
considerar-se biomarcadores per a metalls pesants. La identificació d'aquestes proteïnes i el seu mapatge en
processos cel·lulars específics poden ajudar a aprofundir en els mecanismes tòxics dels metalls pesants en
l'hipocamp. L'anàlisi de la resposta a l'estrès de les cèl·lules HT-22 a les mescles metàl·liques va ser un altre objectiu
de l'estudi (capítol 5) per identificar les proteïnes que intervenen en el mecanisme de neurodegeneració.<br>Environmental exposures are virtually always to complex metal mixtures. Current toxicological studies dictate a largely
metal-by-metal evaluation of exposures and risks in brain, which fails to adequately address potential interactions of
metals in hippocampus region of brain. We evaluated the similar/dissimilar neurotoxicity of each metal in brain that can
give strong support to the mixtures effect in brain (Chapter 1). The scope of our study is to proving the single metal
(Pb, Cd, As, and MeHg) and their mixtures chronic toxicity impact in HT-22 hippocampal cell line by using the in vitro
and system biology methodology. Initially, we performed the cytotoxicity, apoptosis, and genotoxicity assays of single
metals for assessing the toxicity potency of each metal, their mixtures interactions profile in hippocampal cells
(Chapter 2, 3). The obtained results clearly showed the potency of metals MeHg> As>Cd>Pb. Another aim of the
study (Chapter 4) was the heavy metals toxicity in HT- 22 cells using (Pb, Cd, As, and MeHg), as some stress proteins
could be considered as biomarkers for heavy metals. Identification of these proteins and their mapping into specific
cellular processes may help to gain deeper insight into the toxic mechanisms of heavy metals in hippocampus.
Analysis of the stress response of HT-22 cells to metal mixtures was another aim of the study (Chapter 5) to identify
proteins, which are involved in the neurodegeneration mechanism.