Cai Yi, Zhao Li, Qin Yuan, He Yanhuan
Pharmazie. 2015 Jan;70(1):12-6.
Previous studies have suggested that high doses of (-)-epigallocatechin-3-gallate (EGCG) can induce toxicity in the liver, kidneys, and intestine. However, there have been no reports of myocardiotoxicity following treatment with EGCG. In this study, we investiged the proliferation and apoptosis of H9C2 cardiomyocytes treated with high dose of EGCG.
Cell proliferation was measured by CCK8 assay, cell apoptosis rate was evaluated by TUNEL assay, and the expression alterations of Sirtuin 1 (SIRT1) protein was detected by Western blotting.
EGCG inhibits proliferation and induces apoptosis in time- and dose-dependent manner in H9C2 cardiomyocytes. SIRT1 participates in the inhibitory effect of EGCG on cell proliferation and apoptosis induction in H9C2 cardiomyocytes.
This study demonstrates that high doses of EGCG inhibit proliferation and induce apoptosis in H9C2 cardiomyocytes. Down-regulation of SIRT 1 protein expression may be involved.
先前的研究表明,高剂量的(-)-表没食子儿茶素-3-没食子酸酯(EGCG)可在肝脏、肾脏和肠道中诱导毒性。然而,尚无关于EGCG治疗后心肌毒性的报道。在本研究中,我们研究了高剂量EGCG处理的H9C2心肌细胞的增殖和凋亡情况。
通过CCK8法检测细胞增殖,通过TUNEL法评估细胞凋亡率,并通过蛋白质印迹法检测沉默调节蛋白1(SIRT1)蛋白的表达变化。
EGCG以时间和剂量依赖性方式抑制H9C2心肌细胞的增殖并诱导其凋亡。SIRT1参与了EGCG对H9C2心肌细胞增殖的抑制作用和凋亡诱导作用。
本研究表明,高剂量EGCG抑制H9C2心肌细胞的增殖并诱导其凋亡。可能涉及SIRT1蛋白表达的下调。