目的 探究miR-499对心肌缺血/再灌注损伤的保护作用，并从线粒体自噬方面探究其可能机制。 方法 缺血/再灌注（I/R）诱导心肌细胞H9c2（2-1），建立缺氧/复氧（H/R）心肌细胞模型，使用miR-499 mimics和（或）P110处理细胞。将细胞分为BC组、I/R组、I/R + mi组、I/R + NC组、I/R + mi + P110组、I/R + NC + P110组。使用CCK8法检测细胞增殖，流式细胞术检测ROS、线粒体膜电位和细胞凋亡，试剂盒检测MDA、SOD、ATP含量，qRT-PCR和Western blot检测线粒体融合、分裂、自噬相关基因Fis1、Mfn1、Parkin、LC3-Ⅱ、p62和Drp1的mRNA和蛋白表达水平，透射电镜观察线粒体自噬。 结果 miR-499 mimics和/或P110可使I/R诱导的心肌细胞增殖抑制率和凋亡率下降；线粒体膜电位下降、线粒体自噬减少、ATP含量上升；Fis1、Parkin、LC3-Ⅱ和Drp1的基因和蛋白表达水平下降，Mfn1和p62的基因和蛋白表达水平上升；细胞内ROS和MDA含量减少，SOD含量增加。 结论 miR-499可通过降低Drp1介导的线粒体自噬减少氧化应激的发生，从而保护I/R诱导的心肌细胞。

Objective To explore the protective effect of miR?499 on myocardial ischemia?reperfusion injury and its possible mechanism from the aspect of mitochondrial autophagy. Methods Myocardial cell H9c2（2?1） was induced by ischemia/reperfusion （I/R）， and hypoxia/reoxygenation （H/R） myocardial cell model was established. The cells were treated with miR?499 mimics and/or P110. The cells were divided into BC group， I/R group， I/R + mi group， I/R + NC group， I/R + mi + P110 group and I/R + NC + P110 group. Cell proliferation was detected by CCK8 method. ROS， mitochondrial membrane potential and apoptosis were detected by flow cytometry. MDA， SOD and ATP contents were detected by their kit. The mRNA and protein expression levels of mitochondrial fusion， division and autophagy related genes Fis1， Mfn1， Parkin， LC3?Ⅱ， p62 and Drp1 were detected by qRT?PCR and Western blot. Mitochondrial autophagy was observed by transmission electron microscope. Results miR?499 mimics and/or P110 can reduce the proliferation inhibition rate and apoptosis rate of myocardial cells induced by I/R. The mitochondrial membrane potential decreased. The mitochondrial autophagy decreased and the ATP content increased. The gene and protein expression levels of Fis1， Parkin， LC3?Ⅱ and Drp1 decreased， while those of Mfn1 and p62 increased. The content of ROS and MDA in cells decreased， but the content of SOD increased. Conclusions miR?499 can reduce the occurrence of oxidative stress by reducing mitochondrial autophagy mediated by Drp1， thus protecting I/R?induced cardiomyocytes。