Abstract: Objective:Based on the oxidative stress injury model,the protective effect of oxidative stress on hepatocyte injury and its possible mechanism were studied by screening the material basis of ginseng. Methods:A hepatocellular injury model was established by using a hydrogen peroxide solution with the concentration of 25 μmol/L to screen protective effects of total protein,total polysaccharide,total saponin in ginseng. On this basis,cytometry was used to detect the degree of apoptosis,changes in mitochondrial membrane potential,changes in reactive oxygen species,and changes in hepatic glycogen. Changes in hepatic glycogen,superoxide dismutase(SOD),malondialdehyde(MDA),glucose-6-phosphatase(G6P),phosphoenolpyruvate carboxykinase(PEPCK),and atpase were observed by ELISA. Result:After liver cells induced by hydrogen peroxide,cells viability were significantly reduced(P<0.01). By comparing the active ingredients in ginseng,it was found that the protective effect of ginseng polysaccharide was stronger and showed concentration dependence. Compared with the model group,the MDA content in the liver cells of rat for the high dose group of ginseng polysaccharide was significantly decreased(P<0.001). The SOD content in the liver cells of rat for the middle dose group and the high dose group were significantly increased(P<0.05). The content of G6P in the liver cells of rat for the low dose group was significantly increased(P<0.05),and the content of G6P in the middle dose group and the high dose group was significantly increased(P<0.01). The content of PEPCK in the liver cells of rat for the middle dose group was significantly increased(P<0.05)and the content of PEPCK in the high dose group was significantly increased(P<0.01). The atpase content in the liver cells of rat for the low dose group and the middle dose group were significantly increased(P<0.01). The content of hepatic glycogen in the liver cells of rat for middle dose group and high dose group were significantly increased(P<0.05). Conclusion:Ginseng polysaccharide restores the function of mitochondria in hepatocytes by increasing the activity of atpase in hepatocytes and increasing mitochondrial membrane potential. It restores hepatic gluconeogenesis by restoring G6P and PEPCK. At the same time,by increasing SOD and reducing MDA,the damage caused by oxidative stress is weakened. It provides a basis for the subsequent study of oxidative stress-induced liver damage.