Jung Ji-Yeon, Mo Hyun-Chul, Yang Kyu-Ho, Jeong Yeon-Jin, Yoo Hyeon-Gyeong, Choi Nam-Ki, Oh Won-Mann, Oh Hee-Kyun, Kim Sun-Hun, Lee Jin-Ha, Kim Hyun-Jin, Kim Won-Jae
Dental Science Research Institute, School of Dentistry, 2nd Stage of Brain Korea 21 for School of Dentistry, Chonnam National University, Gwang Ju 500-757, South Korea.
Life Sci. 2007 Mar 20;80(15):1355-63. doi: 10.1016/j.lfs.2006.11.033. Epub 2006 Nov 25.
Epigallocatechin-3-gallate (EGCG) is a major constituent of green tea polyphenols. This study was aimed to investigate the possible mechanisms of EGCG-mediated inhibition against apoptosis in rat pheochromocytoma PC12 cells by exposure to CoCl(2). Exposure to CoCl(2) caused the generation of ROS and induced cell death with appearance of apoptotic morphology and DNA fragmentation. However, EGCG rescued the loss of viability in the cells exposed to CoCl(2) and led the reduction of DNA fragmentation and sub-G(1) fraction of cell cycle. Also, EGCG attenuated the CoCl(2)-induced disruption of mitochondrial membrane potential (DeltaPsim), release of cytochrome c from the mitochondria to cytosol and abolished the CoCl(2)-stimulated activities of the caspase cascades, caspase-9 and caspase-3. In addition, EGCG ameliorated the increase in the Bax to Bcl-2 ratio, a marker of apoptosis proceeding, induced by CoCl(2) treatment. Taken together, the present results suggest that EGCG inhibit the CoCl(2)-induced apoptosis of PC12 cells through the mitochondria-mediated apoptosis pathway involved in modulating the Bcl-2 family.
表没食子儿茶素-3-没食子酸酯（EGCG）是绿茶多酚的主要成分。本研究旨在探讨EGCG通过暴露于CoCl₂介导抑制大鼠嗜铬细胞瘤PC12细胞凋亡的可能机制。暴露于CoCl₂会产生活性氧（ROS）并诱导细胞死亡，出现凋亡形态和DNA片段化。然而，EGCG挽救了暴露于CoCl₂的细胞中的活力丧失，并导致DNA片段化减少和细胞周期亚G₁期比例降低。此外，EGCG减弱了CoCl₂诱导的线粒体膜电位（ΔΨm）破坏、细胞色素c从线粒体释放到细胞质，并消除了CoCl₂刺激的半胱天冬酶级联反应、半胱天冬酶-9和半胱天冬酶-3的活性。此外，EGCG改善了CoCl₂处理诱导的凋亡进程标志物Bax与Bcl-2比值的增加。综上所述，目前的结果表明，EGCG通过参与调节Bcl-2家族的线粒体介导的凋亡途径抑制CoCl₂诱导的PC12细胞凋亡。
