NOX2 Antisense Attenuates Hypoxia-Induced Oxidative Stress and Apoptosis in Cardiomyocyte.
NOX2 Antisense Attenuates Hypoxia-Induced Oxidative Stress and Apoptosis in Cardiomyocyte.
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NOX2 反义蛋白可减轻缺氧诱导的心肌细胞氧化应激和细胞凋亡。
DOI：
10.7150/ijms.15177
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发表时间：
2016
影响因子：
3.6
通讯作者：
Shi K
中科院分区：
文献类型：
--
作者：
Yu B;Meng F;Yang Y;Liu D;Shi K
心肌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蛋白水平升高。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明确。在本研究中，我们采用NOX2反义策略，探究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，我们发现腺病毒载体介导的NOX2反义寡核苷酸（ADV - NOX2 - AS）转导可有效沉默心肌细胞中的NOX2，进而减轻缺氧诱导的氧化应激和细胞凋亡。本研究表明基于反义技术的疗法具有潜在应用价值，并证实NOX2是心肌缺血治疗的一个极具潜力的候选靶点。
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.