Objective: To investigate the therapeutic effect of microRNA210 (miRNA-210) modified mesenchymal stem cells (MSCs) on myocardial ischemia-reperfusion injury (MIRI) model rats. Methods: One SD rat was sacrificed, and the lower extremity tibia and femur were isolated. MSCs were cultured by whole bone marrow adherence method to construct miRNA- 210 modified MSCs. 40 SD rats were divided into the sham operation group, model group, MSCs group, and miRNA-210 + MSCs group, with 10 rats in each group. The left anterior descending coronary artery was ligated to prepare a model of myocardial ischemia and reperfusion. After successful modeling, 50 μl of MSCs suspension was injected into the tail vein of the MSCs group, and 50 μl of miRNA-210 modified MSCs suspension was injected into the tail vein of the miRNA-210 + MSCs group. The sham operation group and the model group were injected with the same amount of normal saline. On the 10th day after modeling, the area of myocardial infarction, morphological changes of myocardial tissue, myocardial cell apoptosis rate, and miRNA-210 expression were compared in each group. Results: The area of myocardial infarction and the rate of myocardial cell apoptosis in the model group were significantly higher than those in the sham operation group ( 0.05); The expression level of miRNA-210 in the myocardial tissue of MSCs group was significantly higher than in the MSCs group, model group and sham operation group (P <0.05). HE staining showed that the miRNA-210 + MSCs group had normal morphology of myocardial tissues, more uniform cytoplasmic staining, and arranged neatly myocardial fibers. The inflammatory cell infiltration and interstitial edema of the miRNA-210 + MSCs group were significantly improved compared with the model group and MSCs group. Conclusion: MiRNA-210 modified MSCs can inhibit myocardial cell apoptosis in myocardial ischemia-reperfusion injury model rats, reduce the area of myocardial infarction, and improve pathological damage of myocardial tissue in rats, which has a certain therapeutic effect on myocardial ischemia-reperfusion injury.