AimTo explore whether edaravone(EDA), a novel free radical scavenger, protect H9c2 cells against chemical hypoxia-induced injury.MethodsH9c2 cells were treated with Cobalt chloride (CoCl₂) to set up a chemical hypoxia-induced cellular injury model.Cell viability was detected by cell counter kit (CCK-8).Changes in morphology and amount of apoptotic cells were observed by Hoechst 33258 staining; Intracellular level of reactive oxygen species (ROS) was measured by DCFH-DA staining and photofluorography; Mitochondrial membrane potential (MMP) was tested by JC-1 staining and photofluorography.ResultsExposure of H9c2 cells to 100～1000 μmol/L CoCl₂ for 24 h dose-dependently reduced cell viability.At the range from 12 to 36 h, 800 μmol/L CoCl₂ time-dependently inhibited cell viability.Pretreatment with 10 to 40 μmol/L EDA or with NAC (a ROS scavenger) at 500 to 2000 μmol/L for 1 h prior to exposure to 800 μmol/L CoCl₂ for 24 h dose-dependently blocked the inhibition of cell viability by CoCl₂.Preconditioning with 40 μmol/L EDA for 1 h prior to exposure of H9c2 cells to 800 μmol/L CoCl₂ inhibited not only CoCl₂-induced overproduction of ROS, but also the apoptotic effect and MMP loss induced by CoCl₂.ConclusionsEDA can protect H9c2 cells against CoCl₂-induced injury, which may be associated with its antioxidant effect and protection of MMP.