Inhibition by epigallocatechin gallate of CoCl2-induced apoptosis in rat PC12 cells

Inhibition by epigallocatechin gallate of CoCl2-induced apoptosis in rat PC12 cells
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DOI:
10.1016/j.lfs.2006.11.033
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发表时间:
2007-03-20
期刊:
影响因子:
6.1
通讯作者:
Kim, Won-Jae
Kim, Won-Jae
中科院分区:
医学2区
文献类型:
--
作者:
Jung, Ji-Yeon;Mo, Hyun-Chul;Kim, Won-Jae

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表没食子儿茶素没食子酸酯(Epigallocatechin-3-gallate,EGCG)是绿色茶多酚的主要成分。本研究旨在探讨儿茶素没食子酸酯(EGCG)抑制氯化钴(CoCl 2)诱导的大鼠嗜铬细胞瘤PC 12细胞凋亡的可能机制。CoCl 2暴露引起ROS的产生,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CoCl 2的细胞活力的丧失,并导致DNA片段化和细胞周期亚G(1)分数的减少。此外,表没食子酸酯还能减弱CoCl 2诱导的线粒体膜电位(Delta Psi m)破坏、细胞色素c从线粒体释放到胞浆,并消除CoCl 2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改善了由CoCl 2处理诱导的Bax与Bcl-2比率的增加,这是凋亡进程的标志。综上所述,本研究结果表明,EGCG抑制氯化钴诱导的PC 12细胞凋亡,通过参与调节Bcl-2家族的细胞凋亡通路。(c)2007年爱思唯尔公司All rights reserved.
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 CoCl2. Exposure to CoCl2 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 CoCl2 and led the reduction of DNA fragmentation and sub-G(1) fraction of cell cycle. Also, EGCG attenuated the CoCl2-induced disruption of mitochondrial membrane potential (Delta Psi m), release of cytochrome c from the mitochondria to cytosol and abolished the CoCl2-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 CoCl2 treatment. Taken together, the present results suggest that EGCG inhibit the CoCl2-induced apoptosis of PC12 cells through the mitochondria-mediated apoptosis pathway involved in modulating the Bcl-2 family. (c) 2007 Elsevier Inc. All rights reserved.