Abstract: Objective: To explore the protective effect of ginsenoside on the oxidative stress injury of HepG2 cells induced by hydrogen peroxide(H₂O₂), and to clarify its mechanism. Methods: The HepG2 cells were cultured, and different concentrations (0.1, 0.2, 0.3, 0.4, 0.5, 0.6, 0.7, 0.8 and 1.0 mmol·L^-1) of H₂O₂ were used to induce the HepG2 cell injury. The HepG2 cells were divided into blank group, control group, injury group, ginsenoside control group and ginsenoside protection group. The cells were incubated with 10,20 and 40 μmol·L^-1 ginsenoside RH1, F1, RD, RO and RE for 3 h, and injured with H₂O₂ for 2 h; CCK-8 method was used to detect the cell survival rate, CAA method was used to detect the cell antioxidant capacity, DCFH-DA fluorescence probe method was used to detect the level of reactive oxygen species (ROS), and WST-1 method was used to detect the activity of superoxide dismutase (SOD). Results: The half inhibitory concentration (IC₅₀) of H₂O₂ was 0.4 mmol·L^-1. Compared with injury group, after 10, 20 and 40 μmol·L^-1 ginsenoside RH1, F1, RD, RE and RO pretreatment, the survival rates of HepG2 cells induced by H₂O₂ were increased in varying degrees, and the cell survival rate in ginsenoside F1 protection group was most significantly increased (P<0.05). Compared with control group, in the survival rates of HepG2 cells in 10, 20 and 40 μmol·L^-1 ginsenoside Rh1, F1, RD, and RO protection groups had no significant differences(P>0.05). The half effective concentration(EC₅₀)of ginsenoside F1 was (15.82 ±0.82) μmol·L^-1, and the CAA equivalent was (1275.20±33.90) μmol TE/100 μ mol·L^-1 ginsenoside F1. Compared with control group, the ROS level in HepG2 cells in injury group was significantly increased (P<0.05) and the SOD activity was significantly decreased (P<0.05). Compared with injury group, the ROS level in HepG2 cells in ginsenoside F1 protection group was significantly decreased (P<0.05) and the SOD activity was significantly increased (P<0.05). Conclusion: Ginsenoside F1 can protect the stress injury of HepG2 cells induced by H₂O₂ by the increasing the cell antioxidant capacity, decreasing the ROS level and increasing the SOD activity.

Key words: ginsenoside, hydrogen peroxide, HepG2 cells, oxidative stress, reactive oxygen species