کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
1923407 1048890 2015 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Angiotensin1-7 protects cardiomyocytes from hypoxia/reoxygenation-induced oxidative stress by preventing ROS-associated mitochondrial dysfunction and activating the Akt signaling pathway
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
پیش نمایش صفحه اول مقاله
Angiotensin1-7 protects cardiomyocytes from hypoxia/reoxygenation-induced oxidative stress by preventing ROS-associated mitochondrial dysfunction and activating the Akt signaling pathway
چکیده انگلیسی

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.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Acta Histochemica - Volume 117, Issue 8, October 2015, Pages 803–810
نویسندگان
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