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首页> 外文期刊>Journal of pineal research >Melatonin receptor-mediated protection against myocardial ischemia/reperfusion injury: role of SIRT1.
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Melatonin receptor-mediated protection against myocardial ischemia/reperfusion injury: role of SIRT1.

机译：褪黑素受体介导的抗心肌缺血/再灌注损伤的保护作用：SIRT1的作用。

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摘要

Melatonin confers cardioprotective effect against myocardial ischemia/reperfusion (MI/R) injury by reducing oxidative stress. Activation of silent information regulator 1 (SIRT1) signaling also reduces MI/R injury. We hypothesize that melatonin may protect against MI/R injury by activating SIRT1 signaling. This study investigated the protective effect of melatonin treatment on MI/R heart and elucidated its potential mechanisms. Rats were exposed to melatonin treatment in the presence or the absence of the melatonin receptor antagonist luzindole or SIRT1 inhibitor EX527 and then subjected to MI/R operation. Melatonin conferred a cardioprotective effect by improving postischemic cardiac function, decreasing infarct size, reducing apoptotic index, diminishing serum creatine kinase and lactate dehydrogenase release, upregulating SIRT1, Bcl-2 expression and downregulating Bax, caspase-3 and cleaved caspase-3 expression. Melatonin treatment also resulted in reduced myocardium superoxide generation, gp91(phox) expression, malondialdehyde level, and increased myocardium superoxide dismutase (SOD) level, which indicate that the MI/R-induced oxidative stress was significantly attenuated. However, these protective effects were blocked by EX527 or luzindole, indicating that SIRT1 signaling and melatonin receptor may be specifically involved in these effects. In summary, our results demonstrate that melatonin treatment attenuates MI/R injury by reducing oxidative stress damage via activation of SIRT1 signaling in a receptor-dependent manner.
机译：褪黑素通过减少氧化应激赋予抗心肌缺血/再灌注（MI / R）损伤的心脏保护作用。静默信息调节器1（SIRT1）信号的激活还可以减少MI / R伤害。我们假设褪黑激素可以通过激活SIRT1信号转导来预防MI / R损伤。这项研究调查了褪黑激素治疗对MI / R心脏的保护作用，并阐明了其潜在机制。在存在或不存在褪黑激素受体拮抗剂鲁辛多或SIRT1抑制剂EX527的情况下，将大鼠暴露于褪黑激素治疗，然后进行MI / R手术。褪黑素通过改善缺血后心脏功能，减小梗塞面积，降低凋亡指数，降低血清肌酸激酶和乳酸脱氢酶释放，上调SIRT1，Bcl-2表达并下调Bax，caspase-3和caspase-3表达来赋予心脏保护作用。褪黑素处理还导致心肌超氧化物生成减少，gp91（phox）表达，丙二醛水平和心肌超氧化物歧化酶（SOD）水平升高，这表明MI / R诱导的氧化应激显着减弱。但是，这些保护作用被EX527或luzindole阻断，表明SIRT1信号传导和褪黑激素受体可能特别参与了这些作用。总而言之，我们的结果表明褪黑激素治疗通过以依赖受体的方式激活SIRT1信号传导来减少氧化应激损伤，从而减轻MI / R损伤。

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