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

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