ABSTRACT
Objective: To study the effect of picroside Ⅱ on the expression of microRNA-1 (miR-1) in the H2O2-induced H9c2 cardiomyocytes damage, in order to explore the mechanism of picroside Ⅱ in protecting H9c2 cardiomyocytes from oxidative stress. Method: H9c2 cardiomyocytes were divided into 6 groups:control group, model group (H2O2 200 μmol·L-1), picroside Ⅱ (50, 100, 200 μmol·L-1)+H2O2 (200 μmol·L-1) group and picroside Ⅱ (200 μmol·L-1) group. Picroside Ⅱ group was incubated with picroside Ⅱ for 6 h and then cultured with H2O2 for 2 h. At the end of drugs treatment, the cell viability and the cellular damage of cardiomyocytes were respectively assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) and lactate dehydrogenase (LDH) assays. 4',6-diamidino-2-phenylindole (DAPI) staining and cysteinyl aspartate specific proteinase-3 (Caspase-3) test were used to evaluate cell apoptosis. The mRNA expressions of Caspase-3,B-cell lymphoma-2 (Bcl-2) and miR-1 were measured by Real-time polymerase chain reaction (Real-time PCR). The protein expression of Bcl-2 was detected by Western blot. Result:Compared with the control group, H2O2 could significantly decrease the cell viability and increase the rate of apoptosis, up-regulate mRNA expression of Caspase-3 and miR-1, and down-regulate expression of Bcl-2 in H9c2 cells (PPPPPPPConclusion:Picroside Ⅱ has a protective effect on H9c2 cells from H2O2-induced cardiomyocyte injury by down-regulating mRNA-1 expression and up-regulating the expression of the downstream Bcl-2.