At the same time, NPY-knockout rats exhibited a remarkable decrease in infarct size, serum lactate dehydrogenase activity, cardiomyocyte apoptosis, and caspase-3 expression and activity and a strong improvement in heart contractile function compared with MI rats.
It was found that after miR-34a antagomir reversed FS (%) and EF (%) in MI rats, the messenger RNA (mRNA) and protein levels of Caspase-3 in Sham group and MI + miR-34a antagomir group were significantly lower than those in the MI group (p < 0.05), indicating that the addition of miR-34a antagomir inhibited myocardial cell apoptosis after infarction, while the mRNA and protein levels of Wnt/β-catenin were both higher than those in the MI group.
Transplantation of cardiac Sca-1-positive cells rather than c-Kit-positive cells preserves mitochondrial oxygen consumption of the viable myocardium following myocardial infarction in rats.
Also, terminal deoxynucleotidyl transferase mediated dUTP nick-end labeling staining and the expression of cleaved caspase 3 suggested that MI-induced myocytes apotosis was inhibited by PTHrP 87 to 139.
Furthermore, reconstitution of Sca-1 KO mice with WT Sca-1<sup>+</sup> cells was associated with the reactivation of EMT and improved cardiac function after MI.
Caspase-3 activity was higher in the amygdala (medial and lateral) and hippocampal CA3 region in untreated MI rats, whereas caspase-6 activity was higher in the CA1 region.
<i>In vivo</i>, the MI mice exhibited worse cardiac function by echocardiographic assessment and showed larger myocardial scarring by light microscopy, whereas aliskiren treatment reversed these effects, which were also associated with the changes in caspase-3 and Bcl-2 expression as well as in the number of apoptotic cells.
Erythropoietin administration after myocardial infarction reduced caspase 3 expression (apoptotic activity) and induced neovascularization around the infarct area.