Downregulation of miRNA-30a enhanced autophagy in osthole-alleviated myocardium ischemia/reperfusion injury.

Osthole could alleviate myocardial ischemia/reperfusion (I/R) injury. However, the underlying mechanism remains unclear. In this study, we explored whether microRNA (miR)-30a and its target autophagy marker Beclin-1 involved in the osthole protective role in the rat and cells myocardial I/R injury models. The myocardial damages including increases in myocardial collagen content and cell apoptosis in I/R injury model were observed by Masson's Trichrome Staining and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assays. Osthole significantly inhibited the myocardial damages. Osthole inhibited the induction of miR-30a expression by I/R in rat and hypoxia/reoxygenation (H/R) in myocardial cells. After knockdown, the expression of miR-30a by miR-30a inhibitor, H/R induced cell apoptosis was significantly inhibited. The level of Beclin-1 expression and ratio of LC3BII/LC3BI were inhibited by I/R in rat and H/R in myocardial cells, whereas osthole significantly increased them. Knockdown of miR-30a significantly upregulated the Beclin-1 expression and ratio of LC3BII/LC3BI. Inhibition of autophagy by 3-MA significantly reversed the protective role of osthole in H/R myocardial cell. Therefore, we concluded that the mechanism by which osthole alleviate myocardial I/R injury may be achieved by enhancing the autophagy partially via inhibiting the expression of miR-30a.