N-Acetylcysteine Restores Sevoflurane Postconditioning Cardioprotection against Myocardial Ischemia-Reperfusion Injury in Diabetic Rats.
N-Acetylcysteine Restores Sevoflurane Postconditioning Cardioprotection against Myocardial Ischemia-Reperfusion Injury in Diabetic Rats.
复制标题
N-乙酰半胱氨酸恢复七氟烷后处理对糖尿病大鼠心肌缺血再灌注损伤的心脏保护作用
DOI：
10.1155/2016/9213034
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发表时间：
2016
影响因子：
4.3
通讯作者：
Xia Z
中科院分区：
文献类型：
--
作者：
Lin J;Wang T;Li Y;Wang M;Li H;Irwin MG;Xia Z
七氟醚后处理 (sevo-postC) 心脏保护作用在糖尿病中受到损害，这与氧化应激增加有关。我们假设抗氧化剂 N-乙酰半胱氨酸可能增强或恢复糖尿病患者的 sevo-postC 心脏保护作用。对照或链脲佐菌素诱导的 1 型糖尿病大鼠要么不治疗，要么从注射链脲佐菌素五周后开始用 N-乙酰半胱氨酸治疗 4 周，并在不存在或存在 sevo-postC 的情况下遭受心肌缺血再灌注损伤 (IRI)。糖尿病显示心脏 STAT3 激活 (p-STAT3) 和脂联素减少，同时 FoxO1 和 CD36 增加，这与 sevo-postC 心脏保护作用减少有关。 N-乙酰半胱氨酸和 sevo-postC 协同减少糖尿病组的梗死面积。 N-乙酰半胱氨酸显着增加心脏 p-STAT3，sevo-postC 进一步增强这种作用。在糖尿病大鼠中，N-乙酰半胱氨酸（而不是sevo-postC）降低了心肌FoxO1，而sevo-postC（而不是N-乙酰半胱氨酸）显着增加了糖尿病大鼠的心肌脂联素。结论是，晚期糖尿病大鼠心脏p-STAT3减少，脂联素缺乏，FoxO1和CD36表达增加，这可能是心肌对sevo-postC心脏保护反应性丧失的原因。 N-乙酰半胱氨酸可能通过增强心脏 p-STAT3 和脂联素并减少 Fox1 和 CD36 来恢复 Sevo-postC 对糖尿病的心脏保护作用。
The effect of sevoflurane postconditioning (sevo-postC) cardioprotection is compromised in diabetes which is associated with increased oxidative stress. We hypothesized that antioxidant N-Acetylcysteine may enhance or restore sevo-postC cardioprotection in diabetes. Control or streptozotocin-induced Type 1 diabetic rats were either untreated or treated with N-Acetylcysteine for four weeks starting at five weeks after streptozotocin injection and were subjected to myocardial ischemia-reperfusion injury (IRI), in the absence or presence of sevo-postC. Diabetes showed reduction of cardiac STAT3 activation (p-STAT3) and adiponectin with concomitantly increase of FoxO1 and CD36, which associated with reduced sevo-postC cardioprotection. N-Acetylcysteine and sevo-postC synergistically reduced the infarct size in diabetic groups. N-Acetylcysteine remarkably increased cardiac p-STAT3 which was further enhanced by sevo-postC. N-Acetylcysteine but not sevo-postC decreased myocardial FoxO1 while sevo-postC but not N-Acetylcysteine significantly increased myocardiac adiponectin in diabetic rats. It is concluded that late stage diabetic rats displayed reduction of cardiac p-STAT3, adiponectin deficiency, and increase of FoxO1 and CD36 expression, which may be responsible for the loss of myocardial responsiveness to sevo-postC cardioprotection. N-Acetylcysteine restored Sevo-postC cardioprotection in diabetes possibly through enhancing cardiac p-STAT3 and adiponectin and reducing Fox1 and CD36.