骨髓间充质干细胞分泌的含有miR-663的外泌体改善心肌细胞氧化损伤

X. Xia, Baoan Xu
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引用次数: 0

摘要

本研究评估了miR-663通过从外泌体调节BMSC在心肌细胞氧化损伤中的作用。培养来自大鼠的BMSC并用miR-663模拟物转染以测量miR-663水平、BMSC增殖和凋亡以及cTnT水平。收集上清液中的外泌体。将心肌细胞分为对照组、损伤组和exo-miR-663-BMSC组,然后分析细胞增殖和凋亡活性、miR-663水平、ROS、MDA、SOD和GSH-Px含量以及Nrf2、keap1和HO-1的表达。miR-663模拟物促进BMSC增殖并抑制细胞凋亡,并促使BMSC分化为心肌细胞。miR-663的靶基因是keap1。Exo-miR-663-BMSC组显示心肌细胞增殖增加,凋亡减少,ROS和MDA减少,SOD和GSH-Px水平增加,keap1下调,Nrf2和HO-1上调。此外,外源性miR-633-BMSC显著促进了IRI引起的心脏损伤的恢复。总之,exo-miR-633-BMSC能够改善IRI诱导的心脏损伤。
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miR-663-Containing Exosomes Secreted by Bone Marrow Mesenchymal Stem Cells Ameliorate Cardiomyocyte Oxidative Damage
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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