(−)-Epigallocatechin-3-gallate Induces Apoptosis of Human Hepatoma Cells by Mitochondrial Pathways Related to Reactive Oxygen Species

Abstract

The aim of this study was to investigate the effects of (-)-epigallocatechin-3-gallate (EGCG) on the induction of apoptosis in hepatocarcinoma cell lines in vitro and further examine the molecular mechanisms of EGCG-induced apoptosis. In the present study, it was observed that EGCG rapidly induced apoptosis in hepatocarcinoma SMMC7721 cells. EGCG-induced apoptosis was in association with the attenuation of mitochondrial transmembrane potentials (Deltapsi(m)), the alteration of Bcl-2 family proteins, the release of cytochrome c from mitochondria into the cytosol, and the activation of caspase-3 and caspase-9. Elevation of intracellular reactive oxygen species (ROS) production was also shown during EGCG-induced apoptosis of hepatocarcinoma SMMC7721 cells. The antioxidant N-acetyl-l-cysteine (NAC) significantly reduced ROS production and EGCG-induced apoptosis, suggesting that ROS plays a key role in EGCG-induced apoptosis in hepatocarcinoma SMMC7721 cells. In summary, EGCG-induced apoptosis through mitochondrial pathways, and ROS affected EGCG-induced apoptosis in hepatocarcinoma SMMC7721 cells.