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Tpc1808对H2O2诱导的C6细胞氧化应激性损伤的保护作用

Protective effects of Tpc1808 on rat C6 glioma cells damage induced by oxidative stress

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【作者】 顾芸; 刘炎; 丁斐; 刘梅;

【Author】 Gu Yun, Liu Yan, Ding Fei, Liu Mei△(Jiangsu Key Laboratory of Neuroregeneration, Nantong University, Nantong 226001,China)

【机构】 南通大学江苏省神经再生重点实验室; 南通大学江苏省神经再生重点实验室 南通226001; 南通226001;

【摘要】 目的:研究Tpc1808对H2O2诱导的C6细胞氧化应激性损伤的保护作用。方法:采用细胞培养、基因转染、MTT、LDH、免疫荧光组织化学、Western印迹等技术,以星形胶质瘤C6细胞为研究对象,以H2O2作为氧化应激刺激物,建立细胞损伤模型。结果:当终浓度为100μmol/L的H2O2作用于C6细胞24h后,MTT减小,LDH增加,细胞出现明显凋亡;转染Tpc1808基因的细胞受到保护,grp75表达量增加,与对照组相比有显著差异。结论:Tpc1808基因可以保护H2O2引起的C6细胞氧化应激性损伤,该保护作用可能是通过增加grp75表达实现的。

【Abstract】 Objective:To investigate the protective effects of Tpc1808 gene on hydrogen-peroxide(H2O2)-induced cell apoptosis in rat glioma C6 cells. Methods: MTT assay, LDH release assay and Hoechest stained were used.Results: H2O2 addition reduced the viability of C6 cells and increased the LDH release, but these were prevented by Tpc1808 pre-expressing in C6 cells. C6 cells expressing Tpc1808 significantly decreased apoptosis ratio and apoptosis bodies induced by H2O2 according to FCM analysis using PI as a fluorescent bye and Hoechst staining. Additionally, Tpc1808 induced grp75 protein expression in H2O2-induced C6 cells. Conclusion: These data indicate that Tpc1808 may inhibit ROS-mediated cytotoxic effects through induction of grp75 protein expression.

【关键词】 Tpc1808; 氧化性应激; C6细胞; H2O2;
【Key words】 Tpc 1808; oxidative stress; C6 cell; H2O2;
【基金】 国家自然科学基金项目(30270427)
  • 【文献出处】 解剖学杂志 ,Chinese Journal of Anatomy , 编辑部邮箱 ,2007年04期
  • 【分类号】R363
  • 【下载频次】107
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