期刊
JOURNAL OF BIOMATERIALS AND TISSUE ENGINEERING
卷 12, 期 11, 页码 2141-2146出版社
AMER SCIENTIFIC PUBLISHERS
DOI: 10.1166/jbt.2022.3169
关键词
miR-21; Myocardial Damage; Ischemia-Reperfusion Injury; Bax; BMSCs; Inflammation; OxidativeStress
The study found that overexpression of miR-21 can promote the proliferation of BMSCs, inhibit apoptosis, and accelerate the recovery of damaged myocardium.
This study assessed the effect of miR-21 overexpression on the myocardial injury and inflammation and oxidative stress. Bone marrow mesenchymal stem cells (BMSCs) of rats and lentivirus with pLVX-miR-21 were isolated and assigned into control group, model group, BMSCs group and group of over presentation of miR-21 followed by analysis of the proliferative and apoptotic activity of damaged myocardial cells, miR-21 by RT-PCR and the level of Bcl-2, Bax and VEGF, SOD activity and ROS generation as well as the secretion of IL-6 and TNF-a. H/R group showed significantly upregulated miR-21 expression, decreased cell proliferation, increased Caspase3 activity, reduced Bcl-2, increased Bax as well as decreased VEGF and SOD activity, increased ROS generation and IL-6 and TNF-a secretion. However, BMSC group and miR-21-BMSC group showed the opposite changes of the above mentioned parameters with more changes in miR-21-BMSC group. In con-clusion, the proliferation of BMSC is prompted and apoptosis is restrained with the overexpression of miR-21, leading to accelerated recovery of cardiac injury caused by IRI.
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