Li WenJuan, Nie ShaoPing, Yu Qiang, Xie MingYong
State Key Laboratory of Food Science and Technology, Nanchang University, Nanchang 330047, China.
J Agric Food Chem. 2009 Aug 12;57(15):6685-91. doi: 10.1021/jf901396f.
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.
本研究旨在探讨（-）-表没食子儿茶素-3-没食子酸酯（EGCG）对体外肝癌细胞系凋亡诱导的影响，并进一步研究EGCG诱导凋亡的分子机制。在本研究中，观察到EGCG能迅速诱导肝癌SMMC7721细胞凋亡。EGCG诱导的凋亡与线粒体跨膜电位（Δψm）的减弱、Bcl-2家族蛋白的改变、细胞色素c从线粒体释放到细胞质以及caspase-3和caspase-9的激活有关。在EGCG诱导肝癌SMMC7721细胞凋亡过程中，细胞内活性氧（ROS）的产生也有所增加。抗氧化剂N-乙酰-L-半胱氨酸（NAC）显著降低了ROS的产生和EGCG诱导的凋亡，表明ROS在EGCG诱导肝癌SMMC7721细胞凋亡中起关键作用。总之，EGCG通过线粒体途径诱导凋亡，且ROS影响EGCG诱导肝癌SMMC7721细胞的凋亡。
