Salvianolic acid B induced upregulation of miR-30a protects cardiac myocytes from ischemia/reperfusion injury

BACKGROUND: MicroRNAs (miRNAs) are a novel class of powerful, endogenous regulators of gene expression. This study was designed to ascertain if miR-30a is involved in the cardioprotective actions of salvianolic acid B (Sal B) against myocardial ischemia–reperfusion (I–R) injury through suppression of autophagy. METHODS: Murine myocardial cells that had undergone primary culture were induced by I–R and incubated with Sal B (25, 50, 100 μM) in the presence of a miR-30a mimic or miR-30a inhibitor. Expression of miR-30a, beclin-1, LC3-II and p-Akt protein, cell viability, and lactic acid dehydrogenase (LDH) release were assessed. RESULTS: miR-30a expression was down-regulated remarkably in I–R cells, and this suppression could be reversed by Sal B in a dose-dependent manner. Sal B repressed autophagy in I–R myocardial cells. Sal B improved cell viability and reduced the rate of LDH leakage, which suggested that autophagy suppression was beneficial for cell survival. Knockdown of miR-30a with a miR-30a inhibitor could reverse the anti-autophagy effect of Sal B against I–R injury. Furthermore, we confirmed that Sal B has a protective role in miR-30a-mediated autophagy through the PI3K/Akt signaling pathway, which was abrogated by the PI3K inhibitor LY294002. CONCLUSIONS: These data suggest that miR-30a is involved in Sal B-mediated cardioprotection against I–R injury through the PI3K/Akt signaling pathway. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12906-016-1275-x) contains supplementary material, which is available to authorized users.