Exogenous Glutathione Protects IPEC-J2 Cells against Oxidative Stress through a Mitochondrial Mechanism
文献类型： 外文期刊
第一作者： Chen, Qiuyu
作者： Chen, Qiuyu;Ma, Xianyong;Chen, Qiuyu;Yu, Miao;Tian, Zhimei;Cui, Yiyan;Deng, Dun;Rong, Ting;Liu, Zhichang;Song, Min;Li, Zhenming;Ma, Xianyong;Lu, Huijie;Yu, Miao;Tian, Zhimei;Cui, Yiyan;Deng, Dun;Rong, Ting;Liu, Zhichang;Song, Min;Li, Zhenming;Ma, Xianyong;Lu, Huijie;Yu, Miao;Tian, Zhimei;Cui, Yiyan;Deng, Dun;Rong, Ting;Liu, Zhichang;Song, Min;Li, Zhenming;Ma, Xianyong;Lu, Huijie;Yu, Miao;Tian, Zhimei;Cui, Yiyan;Deng, Dun;Rong, Ting;Liu, Zhichang;Song, Min;Li, Zhenming;Ma, Xianyong;Lu, Huijie;Rong, Ting;Li, Zhenming
作者机构：
关键词： hydrogen peroxide; IPEC-J2 cells; oxidative stress; apoptosis; mitochondrial membrane potential
期刊名称：MOLECULES （ 影响因子：4.927； 五年影响因子：5.11 ）
ISSN：
年卷期： 2022 年 27 卷 8 期
页码：
收录情况： SCI
摘要： The accumulation of reactive oxygen species (ROS) triggers oxidative stress in cells by oxidizing and modifying various cellular components, preventing them from performing their inherent functions, ultimately leading to apoptosis and autophagy. Glutathione (GSH) is a ubiquitous intracellular peptide with multiple functions. In this study, a hydrogen peroxide (H2O2)-induced oxidative damage model in IPEC-J2 cells was used to investigate the cellular protection mechanism of exogenous GSH against oxidative stress. The results showed that GSH supplement improved the cell viability reduced by H2O2-induced oxidative damage model in IPEC-J2 cells in a dose-dependent manner. Moreover, supplement with GSH also attenuated the H2O2-induced MMP loss, and effectively decreased the H2O2-induced mitochondrial dysfunction by increasing the content of mtDNA and upregulating the expression TFAM. Exogenous GSH treatment significantly decreased the ROS and MDA levels, improved SOD activity in H2O2-treated cells and reduced H2O2-induced early apoptosis in IPEC-J2 cells. This study showed that exogenous GSH can protect IPEC-J2 cells against apoptosis induced by oxidative stress through mitochondrial mechanisms.
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