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的治愈作用主要与旁分泌作用有关，而不与转分化有关。数据显示，miR-93-5p的表达在急性心肌梗塞（AMI）后具有心脏保护作用。为了确定形成ADSC的包裹miR-93-5p的囊泡是否具有更好的心脏保护作用，我们在临床水平上研究了炎症因子和miR-30d-5p的表达。大鼠急性心肌梗死模型及体外建立低氧H9c2细胞模型，研究miR-93-5p在缺血性心肌损伤中的保护机制。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，用ADSC衍生的含miR-93-5p的外泌体进行治疗比单纯的外泌体处理对梗塞诱发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的表达可通过分别靶向Atg7和Toll样受体4（TLR4）来显着抑制缺氧诱导的自噬和炎性细胞因子的表达，并证实了Atg7或TLR4的过表达。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衍生的外泌体可通过抑制自噬和炎症反应来预防心脏损伤。