骨髓间充质干细胞（MSCs）分泌的外泌体（Exo）对缺血心肌保护作用越来越受到重视。对间充质干细胞进行基因修饰分泌的Exo作用如何值得研究。本课题预实验发现过表达巨噬细胞移动游走抑制因子（MIF）的人源MSCs（hMSCs）分泌的Exo能抑制心肌细胞衰老；并初步证实AMPK信号通路参与这一过程；高通量测序筛选出Exo的差异表达miRNAs111个，生物信息分析结合文献报道显示has-miR-126-3p起重要作用。我们提出研究假设是过表达MIF的hMSCs分泌的Exo-has-miR-126-3p通过调节AMPK通路抑制心肌细胞衰老，对缺血心肌起保护作用。围绕研究假设，本课题拟进一步研究Exo-has-miR-126-3p抑制心肌细胞衰老的调控机制；Exo-has-miR-126-3p对在体缺血心肌保护作用及其机制。本课题研究成果将对缺血性心肌病治疗提供新思路。

The protection of exosomes (Exo) secreted from human mesenchymal stem cells (MSCs) with over-expression macrophage migration inhibitory factor (MIF) for ischemic cardiomyocites is paid more and more attention. The study of the role of Exo secreting from MSCs with gene modification in myocardial protection is very important. Pre-experimental of this study discovered that Exo secreted from hMSCs with over-expressing MIF inhibited senescence of cardiomyocytes by AMPK pathway; Altogether 111 Exo's differential expression miRNAs were screened by high-throughput sequencing. The biological information method combined with the literature analysis shows that has-miR-126-3p plays an important role. We hypothesized that the Exo-has-miR-126-3p secreted by the hMSCs with over-expressing MIF could protect ischemic myocardium by regulating AMPK pathway. According to the hypothesis of this study, we are going to further research the regulation mechanism of Exo-has-miR-126-3p to inhibit the senescence of cardiomyocytes; and research the effects of Exo-has-miR-126-3p on myocardial protection and its mechanism in ischemic rats. The results of this study will provide new strategy for the treatment of ischemic heart disease.