Abstract:

Objective　To investigate the effects and mechanisms of diosgenin (DG) on hypoxia-induced injury of rat myocardial H9c2 cell.　Methods　Cells were divided into H9c2, DG, Hypoxia and Hypoxia + DG group. Cells were treated with hypoxia for inducing injury, and cells were treated with corresponding concentrations of  DG or solvent. Cell proliferation was measured by CCK8 assay, apoptosis was determined by flow cytometry, the expressions of endoplasmic reticulum stress (ERS)-related proteins (CHOP, cleaved caspase-12, GADD34 and BiP) were determined by western blot. The concentrations of SOD and MDA were also measured. The MI/R rat model was produced, rats were treated with DG intragastrically,recorded heart rate (HR) and mean artery pressure (MAP). The concentrations of serum creatine kinase (CK), SOD and MDA were measured, the tissue injury was determined by HE staining, and the related proteins of ERS was measured by Western blot.   Results  Compared with H9c2 group, the proliferation rate was down-regulated and apoptosis rate was increased in Hypoxia group; compared with the Hypoxia group, proliferation rate was up-regulated and apoptosis rate was decreased in Hypoxia + DG group. Meanwhile, the expression levels of CHOP and Caspase-12 in Hypoxia group were increased compared with the H9c2 group, but the expression levels of GADD34 and BiP were decreased. In addition, hypoxia decreased the concentration of MDA, but increased SOD significantly. DG alleviated the effects of hypoxia. Furthermore, DG enhanced cardiac function of model rats of MI/R, alleviated the injury of myocardial tissue, inhibited the expressions of CHOP and Caspase-12, induced the expressions of GADD34 and BiP, down-regulated the concentration of MDA, and increased SOD in serum of rats. Conclusion  DG attenuates hypocia-induced myocardial cell injury and myocardial injury of model rats of MI/R through inhibiting ERS.

Key words: Hypoxia, Endoplasmic reticulum stress; , Myocardial cell injury, Oxidative stress