Context: Autophagy-apoptosis is the core mechanism of doxorubicin-induced myocardial injury. miR-30a is a pivotal factor in the regulation of autophagy and apoptosis. It remains unclear whether SMI exerts cardioprotective effect by regulating autophagy and apoptosis via miR-30a.

Objective: This study evaluates the effects of SMI on ameliorating doxorubicin-induced myocardial injury.

Materials and Methods: The level of LDH and CK, and the expression of miR-30a was detected. mCherry-EGFP-LC3B double fluorescence was used to observe autophagy flow. Apoptosis was detected by Annexin V/PI staining. Western Blot was used to estimate the expression of autophagy related proteins and apoptosis-related proteins.

Results: Compared with the control group, there were evidently decreased cell viability, elevated level of LDH and CK, down-regulated expression of miR-30a in the model group. Data from Western blot and fluorescence indicated that doxorubicin contributed to the elevated autophagy and apoptosis. Compared with the model group, there were increased cell viability, decreased level of LDH and CK, and up-regulated expression of miR-30a in the Shenmai group and the Shenmai + miR-30a inhibitor group. Meanwhile, the results manifested that there were suppressed autophagy flow accompanied by the down-regulated expression of Beclin-1, LC3-II, LC3-II/LC3-I and up-regulated expression of p62 protein, and declined apoptosis rate accompanied by the up-regulated Bcl2 expression and the down-regulated expression of Bax, Cleaved Caspase-9, Cleaved Caspase-9/Caspase-9, Cleaved Caspase-3, Cleaved Caspase-3/Caspase-3 in the Shenmai group and the Shenmai + miR-30a inhibitor group.

Discussion and Conclusion: Shenmai injection inhibited autophagy and apoptosis via miR-30a, thereby alleviating doxorubicin-induced myocardial injury.