(-)-Epigallocatechin-3-gallate induces apoptosis of human hepatoma cells by mitochondrial pathways related to reactive oxygen species.
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.
Li
WenJuan
W
State Key Laboratory of Food Science and Technology, Nanchang University, Nanchang 330047, China.
Nie
ShaoPing
S
Yu
Qiang
Q
Xie
MingYong
M
D017209:Apoptosis / Q000187:drug effects*; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology; D045744:Cell Line, Tumor; D045304:Cytochromes c / Q000378:metabolism; D006801:Humans; D008113:Liver Neoplasms / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D008928:Mitochondria / Q000737:chemistry / Q000187:drug effects* / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism*
D017382:Reactive Oxygen Species; D002392:Catechin; D045304:Cytochromes c; C045651:epigallocatechin gallate