【Abstract】Objective To investigate the protective effects of sodium thiopental on injury of rat cardiomyocyte H9c2 induced by cobalt chloride (CoCl2) and its potential mechanism.Methods H9c2 cells were treated with CoCl2 to establish an hypoxic injury model, and then the model group was treated with 125 nmol/L, 250 nmol/L, 500 nmol/L sodium thiopental (drugs 1, 2, and 3 groups). The cell survival rate and apoptosis rate were detected by CCK8 assay and flow cytometry, respectively. The expression levels of P21 and Caspase3 proteins were determined by Western blot. The content of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) in H9c2 cells were determined by spectrophotometry, and the level of miR66415p in H9c2 cells induced by CoCl2 was detected by qRTPCR.Results Compared with the control group, the levels of MDA, P21 and Caspase3 in model group increased significantly, the cell survival rate decreased, the apoptosis rate increased, the level of miR66415p and the activity of SOD decreased. Compared with the model group, the levels of MDA, P21 and Caspase3 in group +drug 2 and 3 significantly decreased, the cell survival rate increased, while the apoptosis rate reduced, and the levels of miR66415p and SOD activity increased. Overexpression of miR66415p inhibited the apoptosis of H9c2 cells induced by CoCl2 and improved the survival rate of cells. Inhibition of miR66415p attenuates the protective effect of sodium thiopental on the hypoxia injury of cardiomyocytes H9c2 cells induced by CoCl2.Conclusion Sodium thiopental improves the survival rate, inhibits cell apoptosis and alleviates cell injury of rat cardiomyocytes H9c2 induced by CoCl2 through regulating miR66415p.