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

Figure 4 Cardioprotective effects of hypoxia-preconditioned extracellular vesicles after long periods of hypoxia and ischemia. A: Degree of in situ apoptosis of cardiomyocytes (CMs) in hypoxia and hypoxia-preconditioned extracellular vesicle (HP-EV) groups after a long period (8 h) of hypoxia followed by 12 h of reoxygenation, as determined by the terminal deoxynucleotidyl transferase dUTP nick end-labeling (TUNEL) assay (n = 5); B: Degree of CM apoptosis in the hypoxia and HP-EVs groups after a long period (8 h) of hypoxia followed by 12 h of reoxygenation, as determined by flow cytometry (n = 5); C: Degree of in situ apoptosis of CMs in the myocardial infarction (MI) and HP-EVs groups after a long period of MI [left coronary arteries (LCAs) were ligated for 8 h followed by 12 h of reperfusion], as determined by the TUNEL assay (n = 5); D: Echocardiography was used to examine the heart function of the MI and HP-EVs groups on Day 3 after a long period of MI (LCAs were ligated for 8 h followed by 12 h of reperfusion); ejection fraction and fractional shortening were detected (n = 5). MI: Myocardial infarction; HP-EV: Hypoxia-preconditioned extracellular vesicles.