The Mechanism Of Human Hepatoma MHCC-97H Cells Apoptosis Induced By Ginsenoside-Rk1 And -Rg5

Liver cancer ranks third in the ranking of global malignant tumor mortality,and ranks second in China,seriously threatening the health of human beings in China and the world.Although China has made great progress in research and diagnosis of liver cancer in recent years,the overall prognosis of liver cancer has not improved significantly,and the overall 5-year recurrence rate remains as high as 61.5%.Therefore,it is imperative to develop new drugs for the treatment of liver cancer.Ginsenoside Rk1 and ginsenoside Rg5 are rare ginsenosides,which are active ingredients prepared by processing ginseng with certain anti-cancer,anti-inflammatory and anti-aging activities.The effects of two kinds of ginsenosides on liver cancer cells and the mechanism of inducing apoptosis of liver cancer cells are still unclear.MHCC-97 H cells is a kind of highly metastatic human liver cancer cells with HBsAg(+)and AFP(+)established by Fudan University Liver Cancer Research Institute.They are suitable for the study of the effects of G-Rk1 and G-Rg5 on hepatoma cells.This manuscript aimed to elucidate the molecular mechanism of ginsenoside Rk1 and Rg5(G-Rk1 and G-Rg5)induced apoptosis in MHCC-97 H HCC cell line by a series of cell biology methods such as MTT colorimetry,DAPI staining,flow cytometry,Casapse-3,-8,-9 viability assay,mitochondrial membrane potential assay and Western blotting.we found that:Both G-Rk1 and G-Rg5 can effectively inhibit the proliferation of human hepatoma MHCC-97 H cells in a dose-dependent manner,and the halfinhibitory concentration of G-Rk1 and G-Rg5 were 12.3 ?g/mL and 4.5 ?g/mL,respectively.G-Rk1 and G-Rg5 induced apoptosis through endogenous apoptotic pathways by cause rapid and dramatic translocation of both Bak and Bax,which subsequently triggers mitochondrial cytochrome c release and consequent caspase activation.Caspase-8 is activated too much lower extent than Caspase-9.G-Rk1 and G-Rg5 induced apoptosis can magnify the apoptotic signal through the degradation of c-IAP2 and XIAP.