首页> 外文期刊>Acta Histochemica: Zeitschrift fur Histologische Topochemie >Angiotensin1-7 protects cardiomyocytes from hypoxia/reoxygenation-induced oxidative stress by preventing ROS-associated mitochondrial dysfunction and activating the Akt signaling pathway
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Angiotensin1-7 protects cardiomyocytes from hypoxia/reoxygenation-induced oxidative stress by preventing ROS-associated mitochondrial dysfunction and activating the Akt signaling pathway

机译:血管紧张素1-7通过预防ROS相关的线粒体功能障碍和激活Akt信号通路,保护心肌细胞免受缺氧/复氧诱导的氧化应激

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摘要

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. (C) 2015 Published by Elsevier GmbH.
机译:血管紧张素1-7(Ang1-7)是肾素血管紧张素系统的生物学活性成员,据报道在心肌缺血再灌注诱导的损伤中具有保护作用。但是,这种作用的分子基础还不是很清楚。已经提出氧化应激诱导的心肌细胞凋亡是缺氧/复氧(H / R)损伤的主要结果。这项研究调查了Ang1-7对H / R诱导的大鼠H9C2细胞氧化应激的保护作用。我们的结果表明,Ang1-7(80 nM)处理可通过改善细胞活力和减少细胞凋亡来显着保护细胞免受H / R诱导的氧化损伤。 Ang1-7的保护作用与抑制ROS相关的线粒体功能障碍以及诱导Akt磷酸化有关。这些发现可能显着有助于更好地理解Ang1-7的保护作用,特别是在缺氧/复氧诱导的心脏病中,并为治疗心血管疾病的治疗发展奠定了基础。 (C)2015由Elsevier GmbH发布。

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