NDLI: Exogenous Glutathione Protects IPEC-J2 Cells against Oxidative Stress through a Mitochondrial Mechanism

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Exogenous Glutathione Protects IPEC-J2 Cells against Oxidative Stress through a Mitochondrial Mechanism

Content Provider	MDPI
Author	Chen, Qiuyu Yu, Miao Tian, Zhimei Cui, Yiyan Deng, Dun Rong, Ting Liu, Zhichang Song, Min Li, Zhenming Ma, Xianyong Lu, Huijie
Copyright Year	2022
Abstract	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 (H $_{2}$ O $_{2}$ )-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 H $_{2}$ O $_{2}$ -induced oxidative damage model in IPEC-J2 cells in a dose-dependent manner. Moreover, supplement with GSH also attenuated the H $_{2}$ O $_{2}$ -induced MMP loss, and effectively decreased the H $_{2}$ O $_{2}$ -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 H $_{2}$ O $_{2}$ -treated cells and reduced H $_{2}$ O $_{2}$ -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.
Starting Page	2416
e-ISSN	14203049
DOI	10.3390/molecules27082416
Journal	Molecules
Issue Number	8
Volume Number	27
Language	English
Publisher	MDPI
Publisher Date	2022-04-08
Access Restriction	Open
Subject Keyword	Molecules Hydrogen Peroxide Ipec-j2 Cells Oxidative Stress Apoptosis Mitochondrial Membrane Potential
Content Type	Text
Resource Type	Article

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