Abstract
OBJECTIVE: Metformin, which is commonly recommended drug for managing type II diabetes, has been reported to have anti-cancer properties and may improve the prognosis of some malignancies. Epidemiology studies have shown improved survival in cancer patients using metformin. However, the mechanism behind this phenomenon remains incompletely understood. In our study, Our objective was to investigate how metformin influences the proliferation and apoptosis of hepatocellular carcinoma cells induced with steatosis via palmitic acid and oleic acid. METHODS: We established an in vitro cellular model of non-alcoholic fatty liver disease by inducing lipid accumulation in HepG2 cells through the use of oleic acid and palmitic acid. Oil Red O staining was conducted to observe the distribution of intracellular lipid droplets. Cell proliferation were detected using the BrdU cell proliferation detection kit. Protein expressions were detected by western blot method techniques. RESULTS: We found that metformin reduced cell proliferation in palmitic acid and oleic acid-induced HepG2 cells compared to the control group. Moreover, our western blot data show that metformin treatment changes apoptosis. CONCLUSION: Our results show that metformin inhibits cell viability of steatosis HepG2 cells. These findings may be preliminary for new studies in steatosis HepG2 cells and may provide new therapeutic targets or treatment strategies against hepatocellular carcinoma.