Effects of Exercise Training on the PI3K/Akt Signaling Pathway and miR-21 in Mice with Acute Myocardial Infarction

Abstract

Objectives: The incidence of acute myocardial infarction (MI) is increasing year by year, which seriously affects peoples life quality. It is very important to prevent and treat myocardial infarction. The purpose of this study was to examine how exercise training affects the phosphatidyl-inositol 3-kinase/serine-threonine kinase (PI3K/Akt) signaling pathway in mice with acute myocardial infarction and to determine whether microRNA-21 (miR-21) could also be affected. Methods: 24 C57BL/6 mice were randomly assigned into four groups, including the sham operation group (Sham group) the myocardial infarction Group (MI group), the myocardial infarction + post-exercise training group (MI + TT group), the pre-exercise training + myocardial infarction group (TT + MI group). The expression levels of the b-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), cysteine-aspartic acid protease 3 (Caspase-3) and phosphorylated Akt (p-Akt) were analyzed by western blot, and the mRNA expression levels of collagen type I alpha 1 (Col-1a1), Col-3a1, Fibronectin and miR-21 were detected by reverse transcription polymerase chain reaction (RT-PCR). Results: The protein expression levels of Bax and Caspase-3, which reflect myocardial apoptosis, were inhibited after exercise intervention (p < 0.01), and the Bax protein expression was markedly inhibited in the MI + TT group compared to the TT + MI group (p < 0.01). The protein expression levels of Bcl-2 and p-Akt, indicative of anti-myocardial apoptosis, were increased in the MI + TT and TT + MI groups, with a notable elevation in the MI + TT group (p < 0.01). Cardiac fibrosis indexes (Col1a1, Col3a1, Fibronectin1) in the MI + TT, TT + MI and MI groups were significantly higher than in the Sham group, while the elevation in the MI + TT and TT + MI groups was significantly lower than in the MI group (p < 0.05). The miR-21 expression was increased after myocardial infarction, while the miR-21 expression in the MI + TT and TT + MI groups was lower than in the MI group (p < 0.001). Conclusions: Exercise training can alleviate myocardial cell apoptosis and cardiac fibrosis via the phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt) signaling pathway, and protect myocardial cells. Early exercise after myocardial infarction is more beneficial. Exercise training can reduce the increase of miR-21 and the scope of myocardial infarction.