Aim To explore the effect of edaravone(EDA) on myocardial toxicity –induced by anthracycline antitumor adriamycin(ADR) and the mechanisms underlying. Methods Primary cultured myocardial cells were treated with ADR at different concentrations as a cardiac toxicity model of anthracycline antitumor.EDA was administrated 1 h before ADR as pretreatment.Cell viability was measured by using cell counter kit(CCK-8).The level of intercellular reduced glutathinone(GSH) was detected according to commercial kit.Intercellular reactive oxygen species(ROS) was observed by DCFH-DA staining and photofluorography.The expressions of Cytochrome C and cleaved Caspase-3 were detected by western blot. Results ADR at the concentrations from 1 to 8 mg/L for 24 h damaged myocardial cells in a dose-dependent manner.Preconditioning of 5~20 μmol/L EDA protected myocardial cells against ADR-induced injury,increasing cell survival rate.The preconditioning of EDA inhibited oxidative stress induced by 2 mg/L ADR,increasing the level of GSH and decreasing the content of ROS,and attenuated the expressions of Cytochrome C and cleaved Caspase-3. Conclusion EDA can attenuate the myocardial toxicity induced by ADR,which may be associated with its anti-oxidation and anti-apoptosis action.