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.
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