Esculetin inhibits oxidative stress and apoptosis in H9c2 cardiomyocytes following hypoxiaireoxygenation injury

被引:30
作者
He, Ya [1 ]
Li, Chen [1 ]
Ma, Qiaoya [1 ]
Chen, Songsheng [1 ]
机构
[1] Xi An Jiao Tong Univ, Affiliated Hosp 2, Dept Geriatr Neurol, 157 Xiwu Rd, Xian 710004, Shaanxi, Peoples R China
关键词
Esculetin; Myocardial I/R injury; Oxidative stress; Apoptosis; ISCHEMIA-REPERFUSION INJURY; MYOCARDIAL ISCHEMIA/REPERFUSION INJURY; SIGNALING PATHWAY; PROTECTS; MICE; ACTIVATION; CELLS; HYPOXIA/REOXYGENATION; EXPRESSION; INFLAMMATION;
D O I
10.1016/j.bbrc.2018.04.195
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Esculetin (6,7-dihydroxycoumarin), a natural coumarin compound extracted from natural plants, was reported to be involved in ischemiaireperfusion (I/R) injury. However, the role of esculetin in myocardial injury remains unclear. This study was designed to investigate the protective effects of esculetin on cardiomyocytes induced by hypoxiaireoxygenation (H/R), and explore the underlying mechanisms. Our results showed that esculetin improved the cell viability and decreased lactate dehydrogenase (LDH) release in HER-stimulated H9c2 cells. In addition, esculetin significantly suppressed oxidative stress and apoptosis in H9c2 cells exposed to HER treatment. Exploration of the underlying mechanisms of its action indicated that esculetin enhanced the activation of JAK2/STAT3 pathway in H/R-stimulated H9c2 cells. Taken together, these findings indicated that esculetin inhibits oxidative stress and apoptosis in H9c2 cardiomyocytes following H/R injury through the activation of JAK2/STAT3 pathway. (C) 2018 Published by Elsevier Inc.
引用
收藏
页码:139 / 144
页数:6
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