Epigallocatechin gallate protects H9c2 cardiomyoblasts against hydrogen dioxides-induced apoptosis and telomere attrition
Epigallocatechin gallate protects H9c2 cardiomyoblasts against hydrogen dioxides-induced apoptosis and telomere attrition
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表没食子儿茶素没食子酸酯保护 H9c2 心肌细胞免受二氧化氢诱导的细胞凋亡和端粒磨损
DOI：
10.1016/j.ejphar.2010.05.054
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发表时间：
2010-09-01
影响因子：
5
通讯作者：
Guo, Ci-yi
中科院分区：
文献类型：
--
作者：
Sheng, Rui;Gu, Zhen-lun;Guo, Ci-yi
表没食子儿茶素没食子酸酯（Epigallocatechin gallate，EGCG）是绿色茶中多酚类物质的主要成分，具有良好的心脏保护作用。端粒信号在心功能不全时调节心肌细胞凋亡中发挥作用。本研究旨在探讨表没食子儿茶素没食子酸酯（EGCG）对氧化应激诱导的心肌细胞凋亡和端粒磨损的影响。将H9 c2细胞与50和100 mg/l的EGCG孵育24 h。采用DAPI核染色、电镜、DNA片段电泳和流式细胞术分析200 μ mol/L H2 O2诱导的细胞凋亡。当H9 c2细胞与H2 O2孵育12-24 h时，细胞内和细胞外H2 O2浓度不受EGCG存在的影响。H_2O_2诱导的细胞损伤可见染色质浓缩、DNA断裂和凋亡小体形成。流式细胞仪分析显示细胞凋亡率明显增加。EGCG能显著抑制H2 O2诱导的细胞凋亡形态学改变和细胞凋亡率。H_2O_2作用于H9c_2细胞后，端粒长度逐渐缩短，端粒重复序列结合因子2（TRF 2）蛋白表达逐渐下降，而p53和p21蛋白表达逐渐升高。EGCG显著抑制端粒的磨损。H_2O_2诱导TRF_2丢失和p53、p21上调。这些结果表明，EGCG可能通过抑制端粒依赖的凋亡途径抑制氧化应激诱导的心肌细胞凋亡。(C)2010 Elsevier B. V.保留所有权利。
Epigallocatechin gallate (EGCG), the major component of polyphenols in green tea, has recently attracted considerable attention for its cardioprotective effects. Telomere signalling plays a role in regulating cardiomyocyte apoptosis during cardiac dysfunction. The purpose of this study was to investigate the effects of EGCG on oxidative stress-induced apoptosis and telomere attrition in cardiomyocytes. H9c2 cells were incubated with EGCG, 50 and 100 mg/l, for 24 h. Apoptosis induced by 200 mu mol/l hydrogen dioxide (H2O2) was analyzed by DAPI nuclear staining, electron microscopy, electrophoresis of DNA fragments and flow cytometry. When H9c2 cells were incubated with H2O2 for 12-24 h, the intracellular and extracellular H2O2 concentrations were not affected by the presence of EGCG. Chromatin condensation, DNA fragmentation and apoptotic body formation were observed in H2O2-induced injury. Flow cytometry analysis showed that the apoptotic rate increased remarkably. EGCG significantly inhibited H2O2-induced apoptotic morphological changes and apoptotic rate. When H9c2 cells were incubated with H2O2, the telomere length shortened and the protein expression of telomere repeat-binding factor 2 (TRF2) decreased gradually, while the protein levels of p53 and p21 increased. EGCG significantly inhibited telomere attrition. TRF2 loss and p53, p21 upregulation induced by H2O2. These results suggested that EGCG might suppress oxidative stress-induced cardiomyocyte apoptosis through inhibiting telomere dependent apoptotic pathway. (C) 2010 Elsevier B.V. All rights reserved.