Objective. Necrostatin-1 (Nec-1), an inhibitor of necroptosis, has been reported to protect against myocardial ischemia-reperfusion (MI/R) injury. However, the contribution of the potential antinecroptotic effect of Nec-1 on its infarct limitation and cardiac function improvement effects after MI/R has not been investigated. Methods. The present study investigated the effect of Nec-1 on myocardial infarct size, necroptosis, and cardiac functional recovery in rats subjected to myocardial ischemia-reperfusion (MI/R 30 min/12, 24, 48, and 72 h). Results. The study showed that Nec-1 might reduce myocardial cell death and maintain myoarchitectonic integrity, consequently inhibiting the reactive fibrosis process in rats in myocardial ischemia/late reperfusion. Moreover, the administration of Nec-1 (0.6 mg/kg) at the onset of reperfusion significantly reduced the release of creatine kinase and downregulation of autophagy within 24 h after reperfusion, and there was a significantly positive correlation between them. Conclusion. These results suggest that antinecroptosis treatment may improve the clinical outcomes of patients with ischemic heart disease.

中文翻译：

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Nec-1 对 MI/R 大鼠的心脏保护作用：自噬样细胞死亡的下调

客观。据报道，坏死性凋亡抑制剂 Necrostatin-1 (Nec-1) 可防止心肌缺血再灌注 (MI/R) 损伤。然而，尚未研究 Nec-1 的潜在抗坏死作用对其梗死限制和 MI/R 后心脏功能改善作用的贡献。方法。本研究调查了 Nec-1 对心肌缺血再灌注（MI/R 30 分钟/12、24、48 和 72 小时）大鼠心肌梗死面积、坏死性凋亡和心脏功能恢复的影响。结果. 研究表明，Nec-1 可能减少心肌细胞死亡并维持肌结构完整性，从而抑制大鼠心肌缺血/晚期再灌注的反应性纤维化过程。此外，再灌注开始时给予Nec-1（0.6 mg/kg）可显着降低再灌注后24 h内肌酸激酶的释放和自噬的下调，二者呈显着正相关。结论。这些结果表明抗下垂治疗可能会改善缺血性心脏病患者的临床结局。