The Effect of Carbamazepine Against Glutamate-induced Cytotoxicity in the C6 Cell Line

International Journal of Scientific and Technological Research Pub Date : 2021-09-01 DOI:10.7176/jstr/7-08-09

A. Filiz

{"title":"The Effect of Carbamazepine Against Glutamate-induced Cytotoxicity in the C6 Cell Line","authors":"A. Filiz","doi":"10.7176/jstr/7-08-09","DOIUrl":null,"url":null,"abstract":"Purpose: Recent studies have shown that carbamazepine has positive effects on nervous system. However, its effect on glutamate-induced cytotoxicity in glial cells is still unclear. Our study was designed to investigate the effect of carbamazepine against glutamate-induced cytotoxicity in C6 glial cells and involved mechanisms. Material and Methods: In this study, the C6 glioma cell line was used. Four cell groups were prepared to evaluate the effect of carbamazepine on glial cell death after glutamate-induced cytotoxicity. The control group was without any treatment. Cells in the glutamate group were treated with 10 mM glutamate for 24 hours. Cells in the carbamazepine group were treated with various concentrations (3.75, 7.5, 15, and 30 μM) of carbamazepine for 24 hours. Cells in the carbamazepine + glutamate group were pre-treated with various concentrations (3.75, 7.5, 15, and 30 μM) of carbamazepine for 1 hour and then exposed to 10 mM glutamte for 24 hours. The cell viability was evaluated by XTT assay. Total antioxidant status (TAS), total oxidant status (TOS), tumor necrosis factor alpha (TNF-α), and malondialdehyde (MDA) levels in the cells were measured by commercial kits. Results: Carbamazepine at the concentration of 30 μM significantly increased the cell viability in C6 cells after glutamate-induce cytotoxicity (p < 0.05). CBZ (30 μM) + glutamate significantly increased TOS levels in C6 cells compared to control untreated control cells (p < 0.05), while it did not change TAS level (p > 0.05). Moreover, carbamazepine did not change TNF-α level (p > 0.05) and increased MDA (p< 0.05) level in C6 cells after glutamate-induced cytotoxicity. Conclusion: Carbamazepine decreases glial cell death after glutamate-induced cytotoxicity in C6 cells. While carbamazepine produced protective effective in the acute process, long-term usage may increase oxidative damage and cause cell death. Special Issue of Health Sciences DOI: 10.7176/JSTR/7-08-09","PeriodicalId":14256,"journal":{"name":"International Journal of Scientific and Technological Research","volume":"27 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"International Journal of Scientific and Technological Research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.7176/jstr/7-08-09","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}

引用次数: 1

Abstract

Purpose: Recent studies have shown that carbamazepine has positive effects on nervous system. However, its effect on glutamate-induced cytotoxicity in glial cells is still unclear. Our study was designed to investigate the effect of carbamazepine against glutamate-induced cytotoxicity in C6 glial cells and involved mechanisms. Material and Methods: In this study, the C6 glioma cell line was used. Four cell groups were prepared to evaluate the effect of carbamazepine on glial cell death after glutamate-induced cytotoxicity. The control group was without any treatment. Cells in the glutamate group were treated with 10 mM glutamate for 24 hours. Cells in the carbamazepine group were treated with various concentrations (3.75, 7.5, 15, and 30 μM) of carbamazepine for 24 hours. Cells in the carbamazepine + glutamate group were pre-treated with various concentrations (3.75, 7.5, 15, and 30 μM) of carbamazepine for 1 hour and then exposed to 10 mM glutamte for 24 hours. The cell viability was evaluated by XTT assay. Total antioxidant status (TAS), total oxidant status (TOS), tumor necrosis factor alpha (TNF-α), and malondialdehyde (MDA) levels in the cells were measured by commercial kits. Results: Carbamazepine at the concentration of 30 μM significantly increased the cell viability in C6 cells after glutamate-induce cytotoxicity (p < 0.05). CBZ (30 μM) + glutamate significantly increased TOS levels in C6 cells compared to control untreated control cells (p < 0.05), while it did not change TAS level (p > 0.05). Moreover, carbamazepine did not change TNF-α level (p > 0.05) and increased MDA (p< 0.05) level in C6 cells after glutamate-induced cytotoxicity. Conclusion: Carbamazepine decreases glial cell death after glutamate-induced cytotoxicity in C6 cells. While carbamazepine produced protective effective in the acute process, long-term usage may increase oxidative damage and cause cell death. Special Issue of Health Sciences DOI: 10.7176/JSTR/7-08-09

查看原文本刊更多论文

卡马西平对谷氨酸诱导的C6细胞毒性的影响

目的:近年来研究表明卡马西平对神经系统有积极作用。然而，其对谷氨酸诱导的神经胶质细胞毒性的影响尚不清楚。本研究旨在探讨卡马西平对谷氨酸诱导的C6神经胶质细胞毒性的影响及其机制。材料与方法:本研究采用C6胶质瘤细胞系。制备四组细胞，评价卡马西平对谷氨酸诱导的细胞毒性后神经胶质细胞死亡的影响。对照组不做任何治疗。谷氨酸组细胞用10 mM谷氨酸处理24小时。卡马西平组细胞分别用3.75、7.5、15、30 μM浓度的卡马西平处理24小时。卡马西平+谷氨酸组细胞分别用不同浓度(3.75、7.5、15、30 μM)卡马西平预处理1小时，然后用10 mM谷氨酸处理24小时。采用XTT法测定细胞活力。用商业试剂盒测定细胞中总抗氧化状态(TAS)、总氧化状态(TOS)、肿瘤坏死因子α (TNF-α)和丙二醛(MDA)水平。结果:30 μM卡马西平显著提高谷氨酸诱导细胞毒性后C6细胞的细胞活力(p < 0.05)。与对照组相比，CBZ (30 μM) +谷氨酸可显著提高C6细胞的TOS水平(p < 0.05)，而对TAS水平无显著影响(p > 0.05)。卡马西平未改变谷氨酸诱导的C6细胞TNF-α水平(p > 0.05)，升高MDA水平(p< 0.05)。结论:卡马西平可降低谷氨酸诱导的C6细胞毒性后的胶质细胞死亡。卡马西平在急性过程中具有保护作用，但长期使用可能增加氧化损伤，导致细胞死亡。健康科学特刊DOI: 10.7176/JSTR/7-08-09

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

International Journal of Scientific and Technological Research

自引率

0.00%

发文量