Protective effect of salidroside on cardiomyocyte against apoptosis induced by hypoxia via HIF-1 pathway

AIM: To investigate the inhibitory effect of salidroside(Sal) on cardiomyocyte apoptosis induced by hypoxia and its molecular mechanism.METHODS: Primarily cultured cardiomyocytes of neonatal rats were divided into 6 groups: control group,hypoxia group,hypoxia+different concentrations of Sal pretreatment groups(10,50,100 mg/L),and hypoxia+10-7mol/L insulin group.The cell viability and activities of lactate dehydrogenase(LDH) and creatin kinase(CK) were measured by colorimetric method.The morphologic changes in cardiomyocytes were observed with Hoechst 33258 staining.The apoptosis of cardiomyocytes was detected by flow cytometry and DNA fragmentation.The expression of HIF-1α was determined by immunofluorescence and Western Blot.RESULTS: Compared with hypoxia group,pretreatment with different concentrations of Sal significantly attenuated hypoxia induced cell viability loss and cell death(P0.05) and dramatically decreased the activities of the LDH and CK(P0.01).The Hoechst staining positive cells were significantly decreased with 100 mg/L Sal pretreatment(P0.01).Using flow cytometry,we observed that Sal decreased cell apoptosis induced by hypoxia in a dose-dependent manner.Hypoxia activated the expression of the HIF-1α protein and induced the translocation of HIF-1α.Pretreatment with 100 mg/L Sal significantly up-regulated the level of HIF-1α protein.CONCLUSION: Sal protects cardiomyocytes against apoptosis induced by hypoxia in a dose-dependent manner.This protection is possibly mediated through activating HIF-1α protein expression and inducing the translation of HIF-1α.