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首页> 美国卫生研究院文献>Mediators of Inflammation >N-Acetylcysteine Attenuates Diabetic Myocardial Ischemia Reperfusion Injury through Inhibiting Excessive Autophagy
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N-Acetylcysteine Attenuates Diabetic Myocardial Ischemia Reperfusion Injury through Inhibiting Excessive Autophagy

机译：N-乙酰半胱氨酸通过抑制过度自噬减轻糖尿病性心肌缺血再灌注损伤

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Background. Excessive autophagy is a major mechanism of myocardial ischemia reperfusion injury (I/RI) in diabetes with enhanced oxidative stress. Antioxidant N-acetylcysteine (NAC) reduces myocardial I/RI. It is unknown if inhibition of autophagy may represent a mechanism whereby NAC confers cardioprotection in diabetes. Methods and Results. Diabetes was induced in Sprague-Dawley rats with streptozotocin and they were treated without or with NAC (1.5 g/kg/day) for four weeks before being subjected to 30-minute coronary occlusion and 2-hour reperfusion. The results showed that cardiac levels of 15-F2t-Isoprostane were increased and that autophagy was evidenced as increases in ratio of LC3 II/I and protein P62 and AMPK and mTOR expressions were significantly increased in diabetic compared to nondiabetic rats, concomitant with increased postischemic myocardial infarct size and CK-MB release but decreased Akt and eNOS activation. Diabetes was also associated with increased postischemic apoptotic cell death manifested as increases in TUNEL positive cells, cleaved-caspase-3, and ratio of Bax/Bcl-2 protein expression. NAC significantly attenuated I/RI-induced increases in oxidative stress and cardiac apoptosis, prevented postischemic autophagy formation in diabetes, and reduced postischemic myocardial infarction (all p < 0.05). Conclusions. NAC confers cardioprotection against diabetic heart I/RI primarily through inhibiting excessive autophagy which might be a major mechanism why diabetic hearts are less tolerant to I/RI.
机译：背景。过度自噬是氧化应激增强的糖尿病心肌缺血再灌注损伤（I / RI）的主要机制。抗氧化剂N-乙酰半胱氨酸（NAC）降低心肌I / RI。未知自噬是否可以代表NAC赋予糖尿病心脏保护的机制。方法和结果。在患有链脲佐菌素的Sprague-Dawley大鼠中诱发糖尿病，在不使用或使用NAC（1.5μg/ kg /天）的情况下将其治疗4周，然后进行30分钟的冠状动脉闭塞和2小时的再灌注。结果表明，与非糖尿病大鼠相比，糖尿病患者的心脏15-F2t-异前列腺素水平增加，并且自噬被证明为LC3 II / I比率增加，蛋白P62和AMPK和mTOR表达显着增加，并伴有缺血性增加心肌梗死面积和CK-MB释放，但Akt和eNOS激活降低。糖尿病还与缺血后凋亡细胞死亡增加有关，表现为TUNEL阳性细胞增加，裂解的caspase-3和Bax / Bcl-2蛋白表达比例增加。 NAC显着减弱了I / RI诱导的氧化应激和心脏凋亡的增加，防止了糖尿病中缺血后自噬的形成，并减少了缺血后心肌梗塞的发生（所有p <0.05）。结论。 NAC主要通过抑制过度自噬来赋予针对糖尿病心脏I / RI的心脏保护作用，这可能是糖尿病心脏对I / RI耐受性较低的主要机制。

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