Hepatic Injury Mechanisms Of Tacrine And Effection Of Panaxsaponin To Viability Of Different Hepatocyte

Objective:To investigate the mechanism of liver injury of Tacrine and cell toxicity of several ginsenosides. Methods:First, we determined the half inhibitory concentration(IC50) of tacrine to HepG-2 cells by experiment; then we collected cells and extracted mitochondrial protein, which determined cytokines expression by western blotting; to determine toxicity of Protopanaxadiol, Protopanaxatriol, panoxadiol, ginsenoside Re in hepatoma cells (HepG-2), hepatic stellate cells (t-HSC), normal liver cells (chang liver) by MTT method. Results:After treatment of tacrine, we found that the expression of Bax and Bid increased significantly, and increased with the concentration increase, Cyto C release from mitochondria into the cytoplasm.CONCLUSION:Tacrine induced apoptosis through the mitochondria pathway; Protopanaxadiol when high concentrations was toxic on cells, Protopanaxatriol, panoxadiol, ginsenoside Re almost wasn't toxic on cells.