Edaravone Protects H9c2 Cells Against Chemical Hypoxia-Induced Injury

Aim To explore whether edaravone(EDA),a novel free radical scavenger,protect H9c2 cells against chemical hypoxia-induced injury. Methods H9c2 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. Results Exposure 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. Conclusions EDA can protect H9c2 cells against CoCl2-induced injury,which may be associated with its antioxidant effect and protection of MMP.