Diabetic hearts are more vulnerable to ischemia‐reperfusion injury (I/RI). The activation of nucleotide‐binding oligomerization domain‐like receptor protein 3 (NLRP3) inflammasome can mediate the inflammatory process, and hence might contribute to myocardial I/RI. Activation of autophagy can eliminate excess reactive oxygen species and alleviate myocardial I/RI in diabetes. The present study aimed to investigate whether the activation of autophagy can alleviate diabetic myocardial I/RI through inhibition of NLRP3 inflammasome activation.

中文翻译：

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自噬的激活抑制了核苷酸结合寡聚结构域样受体蛋白 3 炎症小体的激活，并减轻了糖尿病大鼠的心肌缺血再灌注损伤。

糖尿病心脏更容易受到缺血再灌注损伤（I/RI）的影响。核苷酸结合寡聚化结构域样受体蛋白 3 (NLRP3) 炎性体的激活可介导炎症过程，因此可能有助于心肌 I/RI。激活自噬可以消除多余的活性氧，减轻糖尿病患者的心肌 I/RI。本研究旨在探讨自噬的激活是否可以通过抑制 NLRP3 炎性体激活来缓解糖尿病心肌 I/RI。