Exosomes from Adipose-Derived Mesenchymal Stem Cells Alleviates Rat Myocardial Ischemia/Reperfusion Injury by Inhibiting Oxidative Stress and Inflammatory Response

被引:3
|
作者
Du, Wen [1 ]
Wang, Xumin [1 ]
Maimaitiyiming, Dilinuer [1 ]
Sai, Qing [1 ]
Zhao, Guixiang [1 ]
Tuerxun, Gulizhaer [2 ]
机构
[1] Xinjiang Med Univ, Affiliated Hosp 6, Urumqi 830002, Xinjiang, Peoples R China
[2] 947 Hosp Peoples Liberat Army Shule Cty, Special Diag Dept, Kashgar 844200, Xinjiang, Peoples R China
关键词
Myocardial Ischemia/Reperfusion Injury; ADMSCs; Exosomes; Inflammation; EXTRACELLULAR VESICLES;
D O I
10.1166/jbt.2021.2533
中图分类号
Q813 [细胞工程];
学科分类号
摘要
Adipose-derived mesenchymal stem cells (ADMSCs) can inhibite cell apoptosis and promote angiogenesis. Exosomes mainly serve as signaling molecules mediating cell communication. Unlike elaborating research about bone marrow derived mesenchymal stem cells, the role of exosomes secreted by ADMSCs in ischemic diseases is unclear. Oxidative stress and inflammatory response are established to cause ischemia/reperfusion (I/R) injury. We assume that exosomes secreted by ADMSCs may exert a protective role in I/R injury by inhibiting oxidative stress and inflammation. 20-22 months-old rats were used to establish I/R injury model and treated with exosomes from ADMSCs, followed by analysis of infiltration of inflammatory cells, myocardial infarction area, the expression of IL-1B, TNF-alpha, SOD, MDA, NO and 3-NT in the cardiomyocytes. I/R injury resulted in significantly reduced SOD content, elevated NO and 3-NT content, which were all significantly reversed by exosomes from ADMSCs (P < 0.05). Besides, I/R injury did not cause alteration in MDA content which was elevated by exosomes administration (P < 0.05). Further analysis showed that exosomes suppressed IL-1B, TNF-alpha, IL-6 and IL-1 beta levels. Finally, TCC staining displayed that exosomes administration reduced myocardial infarct size. ADMSCs exert a beneficial role in I/R injury by inhibiting oxidative stress and inflammation mediated by IL-1B.
引用
收藏
页码:38 / 43
页数:6
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