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Journal Article
Research Support, Non-U.S. Gov't
(-)-Epigallocatechin-3-gallate induces apoptosis of human hepatoma cells by mitochondrial pathways related to reactive oxygen species.
Journal of Agricultural and Food Chemistry 2009 August 13
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.
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