Fig. 6From: LncRNA-NEAT1 from the competing endogenous RNA network promotes cardioprotective efficacy of mesenchymal stem cell-derived exosomes induced by macrophage migration inhibitory factor via the miR-142-3p/FOXO1 signaling pathwayExosomes derived from MSCs pretreated with MIF modulated oxidant stress to rescue cardiomyocytes. MSCs were transfected with siRNA against lncRNA-NEAT1 or control siRNA-NT and then treated with MIF. The exosomes were collected and added to cardiomyocytes treated with H2O2. Cardiomyocytes were transfected with miR-142-3p mimic, miR-NC mimic, siRNA-FOXO1, or siRNA-NT; treated with exosomeMIF; and subjected to H2O2. Cardiomyocytes, with or without exosomeMIF, were subjected to H2O2. Untreated cardiomyocytes were used as a control. a, b Intracellular ROS production was tested using a ROS detection kit and analyzed using flow cytometry. c Lipid peroxidation was evaluated by MDA formation. d Quantification of 4-HNE levels. e SOD activity was evaluated by colorimetric assay. *P < 0.05 vs. control; ▲P < 0.05 vs. H2O2; ○P < 0.05 vs. H2O2+exosomeMIF+siRNA-LncRNA-NEAT1; □P < 0.05 vs. H2O2+exosomeMIF+ miR-142-3p mimic; ●P < 0.05 vs. H2O2+exosomeMIF+siRNA-FOXO1Back to article page