Eupatilin inhibits the apoptosis in H9c2 cardiomyocytes via the Akt/GSK-3β pathway following hypoxia/reoxygenation injury

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• 作者：Zengyong Qiao^a ; Ya-wei Xu^a ; ^{xuyaweicardio@163.com" class="auth_mail" title="E-mail the corresponding author} ; Jingyu Yang^b ; ^{jingyuphd@126.com" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Eupatilin ; Myocardial ischemia/reperfusion (I/R) ; Oxidative stress ; Apoptosis
• 刊名：Biomedicine & Pharmacotherapy
• 出版年：2016
• 出版时间：August 2016
• 年：2016
• 卷：82
• 期：Complete
• 页码：373-378
• 全文大小：1829 K

文摘

Eupatilin, a pharmacologically active flavone derived from the Artemisia plant species, has been reported to have anti-oxidant, anti-inflammatory, anti-allergic, and neuroprotective activities against cerebral ischemia/reperfusion (I/R). However, the role of eupatilin in myocardial I/R injury remains unclear. In the present study, we aimed to investigate the potential molecular mechanisms against hypoxia/reoxygenation (H/R) induced cardiomyocytes apoptosis in vitro. Our results showed that eupatilin markedly improved the cell viability and decreased lactate dehydrogenase (LDH) release. Eupatilin also suppressed oxidative stress and apoptosis in H9c2 cells after myocardial I/R injury. Furthermore, eupatilin obviously increased the phosphorylation of Akt and GSK-3β in H9c2 cells. Our results suggested that eupatilin could provide significant cardioprotection against myocardial I/R injury, and the potential mechanisms might involve inhibition of cardiomyocyte apoptosis through activating the Akt/GSK-3β signaling pathway.