Extracellular vesicles from hypoxia-preconditioned mesenchymal stem cells alleviates myocardial injury by targeting thioredoxin-interacting protein-mediated hypoxia-inducible factor-1α pathway

Figure 6 Hypoxia-preconditioned extracellular vesicles alleviated hypoxia/reoxygenation-induced apoptosis in vivo. A: Degree of cardiomyocyte (CM) apoptosis in the control, sham, myocardial infarction (MI), normoxic extracellular vesicle (NC-EV), and hypoxia-preconditioned EV (HP-EV) groups after 2 h of left coronary artery (LCA) ligation followed by 12 h of reperfusion, as determined by the terminal deoxynucleotidyl transferase dUTP nick end-labeling assay (n = 5); B: HP-EV cardioprotective effects were assessed in vivo, and MI models were established with LCA ligation for 1 h followed by 12 h of reperfusion. Evans Blue/2,3,5-triphenyltetrazolium chloride staining was used to evaluate the area of viable myocardium in the sham, MI, NC-EV, and HP-EV groups (n = 5); C: Heart function of the sham, MI, NC-EV, and HP-EV groups was evaluated by echocardiography; ejection fraction and fractional shortening were detected (n = 6). All data are expressed as the mean ± SD. ^eP < 0.05, ^fP < 0.01 compared with MI group; ^gP < 0.05, ^hP < 0.01 compared with MI + NC-EVs group. MI: Myocardial infarction; HP-EV: Hypoxia-preconditioned extracellular vesicles; NC-EV: Normoxic extracellular vesicle.