Salvianolic acid B induced upregulation of miR-30a protects cardiac myocytes from ischemia/reperfusion injury. Issue 1 (December 2016)

• Record Type: Journal Article
• Authors: Li, Dan; Wang, Jun; Hou, Jincai; Fu, Jianhua; Liu, Jianxun; Lin, Ruichao
• Is Part Of: BMC complementary and alternative medicine. Volume 16:Issue 1(2016)
• Page Start: 1
• Page End: 9
• Publication Date: 2016-12
• Subjects: Ischemic heart disease -- Salvianolic acid B -- Autophagy -- miR-30a; Alternative medicine -- Periodicals; Complementary Therapies -- Periodicals; 615.505
• DOI: 10.1186/s12906-016-1275-x
• Languages: English
• ISSNs: 1472-6882

Abstract

Abstract 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.