首页> 美国卫生研究院文献>Experimental Diabetes Research >Glycine Protects H9C2 Cardiomyocytes from High Glucose- and Hypoxia/Reoxygenation-Induced Injury via Inhibiting PKCβ2 Activation and Improving Mitochondrial Quality
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Glycine Protects H9C2 Cardiomyocytes from High Glucose- and Hypoxia/Reoxygenation-Induced Injury via Inhibiting PKCβ2 Activation and Improving Mitochondrial Quality

机译:甘氨酸通过抑制PKCβ2活化和改善线粒体质量保护H9C2心肌细胞免受高糖和缺氧/复氧诱导的损伤。

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摘要

Background Patients with diabetes are more vulnerable to myocardial ischemia reperfusion injury (IRI), which is involved in PKCβ2 activation and mitochondrial dysfunction. Glycine has been documented as a cytoprotective agent to attenuate diabetes-related abnormalities and reduce myocardial IRI, but the underlying mechanisms are still unclear. We determined whether glycine could attenuate high glucose- (HG-) and hypoxia/reoxygenation- (H/R-) induced injury by inhibiting PKCβ2 activation and improving mitochondrial quality in cultured H9C2 cells.
机译:背景技术糖尿病患者更容易受到心肌缺血再灌注损伤(IRI)的影响,后者与PKCβ2激活和线粒体功能障碍有关。甘氨酸已被证明是一种细胞保护剂,可减轻糖尿病相关异常并减少心肌IRI,但其潜在机制仍不清楚。我们确定了甘氨酸是否可以通过抑制PKCβ2活化并改善培养的H9C2细胞的线粒体质量来减轻高糖(HG-)和缺氧/复氧(H / R-)诱导的损伤。

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