miRNA-30-3p improves myocardial ischemia via the PTEN/PI3K/AKT signaling pathway.

The aim of this study was to explain the effect and mechanisms of miRNA-30-3p in myocardial ischemia-induced cell apoptosis in vitro and in?vivo studies. In the cell experiment， the H9C2 cells were?divided into the normal control (NC)， and the model， miRNA， and miRNA?+?phosphatidylinositol 3-kinase (PI3K) inhibitor groups. The cell survival rates of the different?groups were measured with?the 3-(4，5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium assay kit;?the lactate dehydrogenase (LDH)， malondialdehyde (MDA) content， and?superoxidedimutase (SOD) activity in the bathing medium were?assayed for the evaluation of myocardial cell injury. The cell apoptosis rate of different?groups was?measured with?flow cytometry analysis. The relative protein?expressions of different?cell groups were evaluated by Western blot analysis. In the vivo study， the Sprague-Dawley rats were divided into four groups: the NC group， the model group， miRNA group， and the (miRNA?+?PI3K inhibitor) group. The?pathological observations， cell apoptosis， LDH， SOD， MDA， and relative protein?expressions were evaluated with?hematoxylin and eosin， enzyme-linked immunosorbent assay， terminal deoxynucleotide transferase dUTP nick-end labeling or immunohistochemical?methods. The results show that miRNA-30-3p had the effect?of?improving?cell apoptosis induced by myocardial ischemia in vitro and in vivo studies by the regulation of the PTEN/PI3K/AKT pathway.