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.
['Li|Dan|D|', 'Wang|Jun|J|', 'Hou|Jincai|J|', 'Fu|Jianhua|J|', 'Liu|Jianxun|J|', 'Lin|Ruichao|R|']
D000818:Animals D001343:Autophagy D001572:Benzofurans D002470:Cell Survival D002478:Cells, Cultured D008297:Male D051379:Mice D008810:Mice, Inbred C57BL D035683:MicroRNAs D032383:Myocytes, Cardiac D019869:Phosphatidylinositol 3-Kinases D015427:Reperfusion Injury D015854:Up-Regulation
Salvianolic acid B miR-30a Autophagy Ischemic heart disease