Gamma-aminobutyric acid enhances miR-21-5p loading into adipose-derived stem cell extracellular vesicles to alleviate myocardial ischemia-reperfusion injury via TXNIP regulation

Figure 3 Gamma-aminobutyric acid-induced adipose-derived mesenchymal stem cells from inguinal adipose tissue exhibits potential in mitigating myocardial injury and improve cardiac function under myocardial ischemia-reperfusion injury conditions in vivo. A: Representative graphs of Evans blue/triphenyltetrazolium chloride stain (n = 5); B: Representative micrographs of myocardial tissue section from the infarcted area stained with terminal deoxynucleotidyl transferase dUTP nick end-labeling (TUNEL) (n = 5) and serum cardiac markers degree of mice (n = 3); C: Representative M-mode images of transthoracic echocardiography, and quantification of left ventricular ejection fraction, left ventricular fraction shortening, left ventricular end diastolic volume and left ventricular end systolic volume (n = 5). ^aP < 0.05, ^bP < 0.01, ^cP < 0.001. AAR: Area at risk; CK: Creatine kinase; cTNT: Cardiac troponin T; CKMB: Creatine kinase-MB; EF: Ejection fraction; EVs: Extracellular vesicles; FS: Fraction shortening; GABA: Gamma-aminobutyric acid; IAT: Inguinal adipose tissue; I/R: Ischemia/reperfusion; IS: Infarct size; LDH: Lactate dehydrogenase; LVEDV: Left ventricular end diastolic volume; LVESA: Left ventricular end systolic volume.