Angiotensin1-7 protects cardiomyocytes from hypoxia/reoxygenation-induced oxidative stress by preventing ROS-associated mitochondrial dysfunction and activating the Akt signaling pathway

详细信息    查看全文

• 作者：Pengjun Zhao ; Fen Li ; ^{lifen1126@outlook.com" class="auth_mail" title="E-mail the corresponding author} ; Wei Gao ; Jing Wang ; Lijun Fu ; Yiwei Chen ; Meirong Huang
• 关键词：Hypoxia/reoxygenation ; Angiotensin1-7 ; Apoptosis ; Mitochondrial dysfunction ; Akt signaling pathway
• 刊名：Acta Histochemica
• 出版年：2015
• 出版时间：October 2015
• 年：2015
• 卷：117
• 期：8
• 页码：803-810
• 全文大小：2371 K

文摘

Angiotensin1-7 (Ang1-7) is a biologically active member of the renin–angiotensin system, which has been reported to exhibit protective effect in myocardial ischemia reperfusion-induced injury. However, the molecular basis of this effect is not well understood. It has been proposed that oxidative stress-induced cardiomyocyte apoptosis is a major consequence of hypoxia/reoxygenation (H/R) injury. This study investigates the protective effect of Ang1-7 against H/R-induced oxidative stress in rat H9C2 cells. Our results showed that Ang1-7 (80 nM) treatment significantly protected cells from H/R-induced oxidative injury via improving cell viability and reducing cell apoptosis. The protective effect of Ang1-7 was associated with the inhibition of ROS-associated mitochondrial dysfunction as well as the induction of Akt phosphorylation. These findings may significantly contribute to better understanding the protective effect of Ang1-7, particularly in hypoxia/reoxygenation-induced heart diseases and form the basis in the therapeutic development in treating cardiovascular diseases.