Abstract
The aim of the present study was to determine the cardioprotective mechanisms by which micro (mi)RNA-30e protects the heart from myocardial ischemia/reperfusion injury (MI/R) and to explore the signaling pathways that may confer protection for the heart and be potential therapeutic targets. It was demonstrated that miRNA‑30e expression was decreased in patients with MI/R. In H9C2 cells, silencing (si)miRNA‑30e significantly inhibited cellular apoptosis, the expression of apoptosis regulator BAX (Bax) and caspase‑3 activity. It also significantly increased the expression of microtubule‑associated proteins 1A/1B light chain 3B, p62, Beclin‑1, neurogenic locus notch homolog protein‑1 (Notch1), Hes1 and phosphorylated‑protein kinase B (p‑Akt), and decreased the expression of inducible NO synthase (iNOS) and proteins associated with oxidative stress. The inhibition of autophagy following treatment with 3‑methyladenine significantly reversed the effect of si‑miRNA‑30e on apoptosis, Bax, caspase‑3, iNOS and oxidative stress in H9C2 cells. The promotion of Notch1 expression increased the effect of si‑miRNA‑30e on apoptosis, Bax, caspase‑3, iNOS, Notch1, Hes1 and p‑Akt protein expression and oxidative stress in H9C2 cells. Taken together, these results indicate that miRNA‑30e protects the heart from MI/R via autophagy and the Notch1/Hes1/Akt signaling pathway.