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

2009; American Chemical Society; Volume: 57; Issue: 15 Linguagem: Inglês

10.1021/jf901396f

1520-5118

Wenjuan Li, Shaoping Nie, Qiang Yu, Mingyong Xie,

Tannin, Tannase and Anticancer Activities

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 (Δψm), 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.