Heat shock protein 90 protects H9C2 cardiac cells against CoCl2-induced injuries.

Objective To investigate the protection of heat shock protein 90(HSP90)against H9C2 cardiac cell injuries induced by cobalt chloride(CoCl2).Method H9C2 cells were treated with CoCl2 at different concentrations to set up the chemical hypoxia-induced cardiomyocyte injury model.Cell viability was measured by using cell counter kit(CCK-8).The expression of HSP90 was tested by Western-blot assay.Intracellular reactive oxygen species(ROS)was evaluated by 2',7'-dichlorfluorescein-diacetate(DCFH-DA) staining and photofluorography.The inhibitory rate of superoxide dismutase(SOD) was detected by commercial kit.Result H9C2 cell viability was dose-dependently damaged by CoCl2 at concentrations from 400 to 1000 μmol / L for 36 h.The expression of HSP90 in H9C2 cells was unregulated by 600 μmol / L CoCl2 in a time-dependent manner.17-allylamino-17-demethoxygeldanamycin(17AAG)(an inhibitor of HSP90)at 2-16 μmol / L promoted dose-dependently the inhibition of 600 μmol / L CoCl2 on the cell viability.17AAG at 2 μmol / L alone did not damage H9C2 cells,but significantly enhanced overproduction of ROS induced by CoCl2,and increased the CoCl2-induced inhibition of SOD activity.Conclusion Upregulation of HSP90 expression may be one of the endogenous defense mechanisms for H9C2 cells against chemical hypoxia.