Adipose-derived stromal cells (ADSCs) have been considered as an attractive therapeutic tool. Accumulating evidence indicates that the healing effects of ADSCs are mainly related to paracrine action rather than transdifferentiation. Data show that the expression of miR-93-5p has a cardio-protective effect after acute myocardial infarction (AMI). To identify whether miR-93-5p-encapsulating exosomes that form ADSCs have a better cardio-protective effect, we investigated the inflammatory factors and miR-30d-5p expression in clinical levels. A rat model of AMI and an in vitro model of hypoxic H9c2 cells were established to study the protective mechanism of miR-93-5p in ischemia-induced cardiac injury. The results show that the expression of inflammatory cytokines and miR-93-5p were increased following AMI in both patients and animal models. Moreover, treatment with ADSC-derived miR-93-5p-containing exosomes has a greater protective effect on infarction-induced myocardial damage than simple exosome processing. Furthermore, in vitro experiments confirmed that the expression of miR-93-5p can significantly suppress hypoxia-induced autophagy and inflammatory cytokine expression by targeting Atg7 and Toll-like receptor 4 (TLR4), respectively, and was confirmed with Atg7 or TLR4 overexpression. The results also show that autophagy activation can promote inflammatory cytokine expression indirectly. Taken together, these results suggest that the miR-93-5p-enhanced ADSC-derived exosomes prevent cardiac injury by inhibiting autophagy and the inflammatory response.

脂肪源性基质细胞（ADSC）被认为是一种有吸引力的治疗工具。越来越多的证据表明，ADSCs 的愈合作用主要与旁分泌作用有关，而不是与转分化有关。数据显示，miR-93-5p的表达在急性心肌梗死（AMI）后具有心脏保护作用。为了确定形成 ADSC 的封装 miR-93-5p 的外泌体是否具有更好的心脏保护作用，我们研究了临床水平的炎症因子和 miR-30d-5p 表达。建立AMI大鼠模型和体外缺氧H9c2细胞模型，研究miR-93-5p对缺血性心脏损伤的保护机制。结果表明，在患者和动物模型中，AMI 后炎症细胞因子和 miR-93-5p 的表达均增加。此外，与简单的外泌体处理相比，使用 ADSC 衍生的含有 miR-93-5p 的外泌体进行治疗对梗死引起的心肌损伤具有更大的保护作用。此外，体外实验证实，miR-93-5p的表达可以分别通过靶向Atg7和Toll样受体4（TLR4）来显着抑制缺氧诱导的自噬和炎症细胞因子的表达，并通过Atg7或TLR4的过表达得到证实。研究结果还表明，自噬激活可以间接促进炎症细胞因子的表达。综上所述，这些结果表明 miR-93-5p 增强的 ADSC 衍生的外泌体通过抑制自噬和炎症反应来预防心脏损伤。