The Mechanism Study Of Apoptosis Induced By EGCG Treatment On HepG2 Cells

Objective :To investigate the mechanism study of apoptosis induced by epigallocatechin-3-gallate( EGCG) treatment on HepG2 cells will provide theory evidence in both prevention and cure tumor.Methods:HepG2 cells were propagated in a serum-free in vitro model with different content EGCG treatment for 24 hours. Cell proliferation and cell viability were determined by MTT assay. Cell toxicity was deter- mined by lactate dehydrogenase assay. Cell apoptosis was determined by flow cytometer in PI staining. The human mRNA levels of p38MAPK and Caspase-8 in HepG2 cells were determined by RT-PCR. Protein levels of pp38MAPK and Caspase-8 in the HepG2 cells were determined by Western blot.Results:1. Compared with control groups, 20,40,60μmol/L EGCG caused statistically significant inhabition of cell viability by the dose depend- ence without cell toxicity (P < 0.01).2. 20,40 and 60μmol/L EGCG induce apoptotic in a concentration- dependents manner and cell apoptotic percentage induced by EGCG was 3.6%,15.2% and 31.3% respectively.3. 20,40 and 60μmol/L EGCG cause statistically significant increases mRNA expression of p38MAPK and Caspase-8 in HepG2 cells compared with control groups (P < 0.01).4. 20,40 and 60μmol/L EGCG cause statistically significant incr- eases protein expression of p38MAPK and Caspase-8 in HepG2 cells compared with control groups (P < 0.01). Conclusion:EGCG induces apoptosis of HepG2 cells probably by pp38MAPK to activate death receptor Fas/FasL pathway.