糖尿病状态下，七氟醚后处理（sevoflurane postconditioning, SPostC）的心肌保护作用减弱。文章就近年来SPostC在心肌缺血再灌注损伤（myocardial ischemia reperfusion injury, MIRI）中作用的最新研究进展进行综述，着重讨论糖尿病减弱SPostC心肌保护作用的分子机制，其中包括磷脂酰肌醇‑3‑激酶 （phosphoinositide 3‑kinase, PI3K）/蛋白激酶B（protein kinase B, Akt）、缺氧诱导因子‑1α（hypoxia‑inducible factor‑1α, HIF‑1α）和酪氨酸蛋白激酶2（janus kinase 2, JAK2）/信号转导因子和转录激活因子3（signal transducer and activator of transcriptions 3, STAT3）等多条信号通路的受损及氧化应激和动力相关蛋白1（dynamin related protein 1, DRP1）等诱导的线粒体损伤，讨论了恢复SPostC对糖尿病心肌保护作用的策略，以期为恢复糖尿病心肌对SPostC的敏感性提供新的治疗靶点。
The cardioprotective effect of sevoflurane postconditioning (SPostC) is weakened in the diabetic state. In this review, we summarize the research progress on the roles of SPostC in myocardial ischemia reperfusion injury (MIRI) and focus on the molecular mechanisms by which diabetes attenuates its cardioprotective effect. Numerous impaired signaling pathways are researched, including phosphoinositide 3‑kinase (PI3K)/protein kinase B (Akt), hypoxia‑inducible factor‑1α (HIF‑1α) and janus kinase 2 (JAK2)/signal transduction factor and transcription activator 3 (STAT3) signaling. In addition, oxidative stress and dynamin related protein 1 (DRP1) induced mitochondrial dysfunction are also involved in heart tissue damage. In addition, the present review discusses the strategies for restoring the protective effect of SpostC on diabetic myocardium, which may provide a new therapeutic target.
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