Razi Herbal Medicines Research Center, Lorestan University of Medical Sciences Khorramabad, Iran.
Cardiovascular Research Center, Shahid Rahimi Hospital, Lorestan University of Medical Sciences, Khoramabad, Iran.
Arch Physiol Biochem. 2022 Jun;128(3):830-835. doi: 10.1080/13813455.2020.1729816. Epub 2020 Mar 6.
Oxidative stress, has been shown to play an important role in the pathophysiology of cardiac remodelling and heart failure. The aim of study is effect of arginine vasopressin (AVP) on apoptosis of cardiomyocyte via its receptors.
The cell viability effect of AVP in H9C2 cardiomyocytes was assayed using the MTT method. The transcription and translation level of apoptosis genes (Bax, Bcl-2, caspase-3) were discovered with qRT-PCR and western blotting.
The results showed that vasopressin could reduce apoptosis in cardiomyocytes cell line through downregulation of caspase-3, BAX and upregulation of Bcl-2 ( < .001). Also, there was a decrease in anti-apoptosis effect of vasopressin when V1A and OTR receptors were blocked with their antagonists.
These results suggest that activation of V1A and OTR receptors in H9C2 cells mediate protective effect of vasopressin via regulating apoptosis marker that lead to cell survival under conditions of stress oxidative.Key pointAVP may contribute to the improvement of heart ischaemia through its actions on V1A and OTR receptors.
氧化应激在心肌重构和心力衰竭的病理生理学中起着重要作用。本研究旨在通过其受体研究血管加压素(AVP)对心肌细胞凋亡的影响。
用 MTT 法检测 AVP 对 H9C2 心肌细胞活力的影响。用 qRT-PCR 和 Western blot 检测凋亡基因(Bax、Bcl-2、caspase-3)的转录和翻译水平。
结果表明,加压素通过下调 caspase-3、BAX 和上调 Bcl-2 减少心肌细胞系中的细胞凋亡(<0.001)。此外,当用其拮抗剂阻断 V1A 和 OTR 受体时,加压素的抗凋亡作用减弱。
这些结果表明,H9C2 细胞中 V1A 和 OTR 受体的激活通过调节凋亡标志物介导加压素的保护作用,从而导致应激氧化条件下的细胞存活。
AVP 可能通过其对 V1A 和 OTR 受体的作用有助于改善心脏缺血。