Effect of puerarin on apoptosis of human hepatocellular carcinoma cells under oxidative stress and its mechanisms.

Purpose: To investigate the effect puerarin on the apoptosis of human hepatocellular carcinoma cells induced by hydrogen peroxide and its mechanism. Methods: Experiments were divided into control group, model group, and puerarin group. Normal saline (200 mu mol/L) was used in the control group, 200 mu mol/LH2O2 was used to induce oxidative stress in the model group, and 25 mu mol/L 50 mu mol/L, and 100 mu mol/L, puerarin were used in the puerarin group to treat hepatocellular carcinoma SMMC-7721 cells for 24 h on the basis of 200 mu mol/LH2O2, respectively. Contents of malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) in SMMC-7721 cells were determined by colorimetry. Apoptotic rate of SMMC-7721 cells was determined by flow cytometry. Results: Compared with the control group, MDA content in the H2O2 group increased significantly, and SOD activity and GSH content decreased significantly Compared with the control group, SOD activity and GSH content in SMMC-7721 cells of puerarin group decreased significantly (p<0.05). Compared with the H2O2 group, content of MDA in SMMC-7721 cells of the puerarin group decreased significantly, while SOD activity and GSH content (p<0.05) increased significantly. Activity of SOD and content of GSH in SMMC-7721 cells incubated with 50 mu mol/L and 100 mu mol/L puerarin were significantly higher than that in cells treated with 25 mu mol/L puerarin (p<0.05). Activity of SOD and content of GSH in SMMC-7721 cells incubated with 100 mu mol/L puerarin were significantly higher than those in cells treated with 50 mu mol/L puerarin (p <0.05). Apoptosis rate of SMMC-7721 cells incubated with different concentrations of puerarin was significantly lower than that of the H2O2 group (p <0.05). Conclusion: Puerarin has protective effect on hepatocellular carcinoma SMMC-7721 cells under oxidative stress. It is suggested that puerarin should be carefully used when the proliferation of hepatocellular carcinoma cells results in the production of large amounts of ROS.