Myocardial infarction (MI) is a vital cause of death and disability globally. The primary treatment for diminishing acute myocardial ischemic injury is myocardial reperfusion, which may induce cardiomyocyte death. Our aim is to unravel the mechanism of sevoflurane (Sev) in microRNA-219a (miR-219a)-mediated regulation of absent in melanoma 2 (AIM2) and TLR4/MyD88 pathway during myocardial ischemia/reperfusion (I/R). The area of MI and apoptosis of cardiomyocytes of the developed mouse model were evaluated by TTC staining and TUNEL, respectively. After the determination of miR-219a as our target using microarray analysis, miR-219a atagomiR was used to treat the mouse model. The luciferase assay verified whether miR-219a targeted AIM2, and the miR-219a and AIM2 expression in myocardial tissues was detected by RT-qPCR and Western blot. miR-219a was significantly increased in myocardial tissues from mice treated with Sev, and the area of MI and cardiomyocyte apoptosis were decreased as a consequence. The miR-219a inhibitor reversed the action of Sev. Moreover, overexpression of AIM2 or induction of the TLR4 pathway aggravated myocardial I/R injury alleviated by miR-219a. All in all, the treatment of Sev upregulated miR-219a expression, which blocked the TLR4 pathway by targeting AIM2 and attenuated cardiomyocyte apoptosis in myocardial I/R mouse model.

心肌梗塞 (MI) 是全球死亡和残疾的重要原因。减轻急性心肌缺血损伤的主要治疗方法是心肌再灌注，这可能会导致心肌细胞死亡。我们的目标是解开七氟醚 (Sev) 在 microRNA-219a (miR-219a) 介导的黑色素瘤 2 (AIM2) 和 TLR4/MyD88 通路中心肌缺血/再灌注 (I/R) 通路调节中的机制。分别通过 TTC 染色和 TUNEL 评估开发的小鼠模型心肌细胞的 MI 面积和凋亡。在使用微阵列分析确定 miR-219a 作为我们的靶标后，使用 miR-219a atagomiR 治疗小鼠模型。荧光素酶检测验证了 miR-219a 是否靶向 AIM2，并通过 RT-qPCR 和蛋白质印迹检测心肌组织中 miR-219a 和 AIM2 的表达。用 Sev 治疗的小鼠心肌组织中 miR-219a 显着增加，因此 MI 面积和心肌细胞凋亡减少。miR-219a 抑制剂逆转了 Sev 的作用。此外，AIM2 的过表达或 TLR4 通路的诱导加重了 miR-219a 减轻的心肌 I/R 损伤。总而言之，Sev 的治疗上调 miR-219a 表达，其通过靶向 AIM2 阻断 TLR4 通路并减弱心肌 I/R 小鼠模型中的心肌细胞凋亡。