Protective effect of Cordyceps polysaccharide on hydrogen peroxide-induced mitochondrial dysfunction in HL-7702 cells

Liu,Yunxia; E,Qiukai; Zuo,Ji; Tao,Yanyan; Liu,Wen

doi:10.3892/mmr.2012.1248

Protective effect of Cordyceps polysaccharide on hydrogen peroxide-induced mitochondrial dysfunction in HL-7702 cells

Authors:
- Yunxia Liu
- Qiukai E
- Ji Zuo
- Yanyan Tao
- Wen Liu
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Affiliations: Department of Cellular and Genetic Medicine, Shanghai Medical College, Fudan University, Shanghai 200032, P.R. China, Institute of Liver Diseases, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 310000, P.R. China
Published online on: December 21, 2012 https://doi.org/10.3892/mmr.2012.1248
Pages: 747-754

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Abstract

Multiple reports have suggested that reactive oxygen species (ROS) are implicated in hepatic fibrosis and that they are capable of causing hepatocyte apoptosis in hepatic fibrosis by causing oxidative damage to the liver. Thus, the study of antioxidant compounds may shed light on the treatment of hepatic fibrosis. The aim of the current study was to investigate the protective effects of Cordyceps polysaccharide (CPS), a major antioxidative component of Cordyceps militaris, on hydrogen peroxide (H2O2)-induced cell apoptosis. The data showed that CPS markedly inhibited H2O2-induced mitochondrial dysfunction, lowered cell viability, increased the apoptotic rate, boosted ROS production, decreased mitochondrial membrane potential (MMP), reduced the intracellular adenosine triphosphate (ATP) level, increased the Bax/Bcl-2 ratio and promoted cytochrome C (Cyt C) release. These results indicated that CPS protected HL-7702 cells, which are used as the main model of hepatic fibrosis, against H2O2-induced mitochondrial dysfunction by decreasing ROS production and regulating mitochondrial apoptotic signaling through the Cyt C, Bax and Bcl-2 apoptosis-related proteins.

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