This study assesses the role of miR-663 in the oxidative damage in myocardial cells through regulating BMSC from exosome. BMSC from rats was cultivated and transfected with miR-663 mimics to measure miR-663 level, BMSC proliferation and apoptosis and cTnT level. Exosome in supernatant
was collected. The myocardial cells were assigned into control set, damage set and exo-miR-663-BMSC set followed by analysis of cell proliferative and apoptotic activity, miR-663 level, ROS, MDA, SOD and GSH-Px content as well as the expression of Nrf2, keap1 and HO-1. BMSC proliferation was
prompted and apoptosis was restrained by miR-663 mimics and BMSC was prompted to be differentiated into myocardial cells. The target gene of miR-663 was keap1. Exo-miR-663-BMSC set showed increased myocardial cell proliferation and decreased apoptosis, reduced ROS and MDA as well as increased
SOD and GSH-Px level along with downregulation of keap1 and upregulated of Nrf2 and HO-1. In addition, the recovery of heart injury caused by IRI was significantly prompted by exo-miR-663-BMSC. In conclusion, exo-miR-663 BMSC is capable to ameliorate heart injury induced by IRI.
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