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NOX2反义核酸减轻缺氧诱导的心肌细胞氧化应激和凋亡。

NOX2 Antisense Attenuates Hypoxia-Induced Oxidative Stress and Apoptosis in Cardiomyocyte.

作者信息

Yu Bo, Meng Fanbo, Yang Yushuang, Liu Dongna, Shi Kaiyao

机构信息

Department of cardiology, China-Japan union hospital of Jilin University, Changchun, Jilin, 130033, P.R. China.

出版信息

Int J Med Sci. 2016 Jul 27;13(8):646-52. doi: 10.7150/ijms.15177. eCollection 2016.

DOI:10.7150/ijms.15177
PMID:27499697
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4974913/
Abstract

Heart ischemia is a hypoxia related disease. NOX2 and HIF-1α proteins were increased in cardiomyocytes after acute myocardial infarction. However, the relationship of the hypoxia-induced HIF-1α. NOX2-derived oxidative stress and apoptosis in cardiomyocyte remains unclear. In the current study, we use NOX2 antisense strategy to investigate the role of NOX2 in hypoxia-induced oxidative stress and apoptosis in rat cardiomyocytes. Here, we show that transduction of ADV-NOX2-AS induces potent silencing of NOX2 in cardiomyocytes, and resulting in attenuation of hypoxia-induced oxidative stress and apoptosis. This study indicates the potential of antisense-based therapies and validates NOX2 as a potent therapeutic candidate for heart ischemia.

摘要

心脏缺血是一种与缺氧相关的疾病。急性心肌梗死后,心肌细胞中的NOX2和HIF-1α蛋白增加。然而,缺氧诱导的HIF-1α、NOX2衍生的氧化应激与心肌细胞凋亡之间的关系仍不清楚。在本研究中,我们采用NOX2反义策略来研究NOX2在大鼠心肌细胞缺氧诱导的氧化应激和凋亡中的作用。在此,我们表明,转导ADV-NOX2-AS可有效沉默心肌细胞中的NOX2,并减轻缺氧诱导的氧化应激和凋亡。本研究表明了基于反义的治疗方法的潜力,并验证了NOX2作为心脏缺血有效治疗候选物的可能性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3580/4974913/1b5ed3247a9b/ijmsv13p0646g005.jpg
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