Abstract: ob＜x＞jective Through vivo and vitor experiments, the protective effect of daidzein on myocardial injury induced by doxorubicin and its mechanism were discussed. Methods SD rats were randomly divided into 4 groups: Ctrl group, Daid group, Dox group and Daid+Dox group. After 6 weeks of intervention, the ratio of heart weight to body weight and body length to tail length of rats were measured, and myocardial enzyme activity in serum, like LDH and CK, was detected by colorimetry. The myocardial tissue structure and Caspase-3 protein ex＜x＞pression were detected by H-E staining and immunohistochemistry. DHE staining was used to detect the DHE fluorescence ex＜x＞pression level of H9C2 in cardiomyocytes of different groups, and Western blotting was used to detect the ex＜x＞pression level of apoptotic protein Caspase-3. Results Compared with Ctrl group, Dox increased the ratio of heart weight to body weight and decreased the ratio of body length to tail length, but there was no statistical difference between the two groups (P>0.05). Serum myocardial injury indexes of Dox group were significantly higher than those of Ctrl group (P<0.01), and the above indexes in Daid+Dox group were significantly lower than those in Dox group (P<0.01).In Dox group, myocardial fibers were disordered, disintegrated and apoptosis increased, while in Daid+Dox group, the above conditions were significantly improved. At the cell level, the fluorescence ex＜x＞pression of DHE and the ex＜x＞pression of Caspase-3 protein were significantly enhanced after DOX treatment, while the above indexes were reversed in Daid+Dox group (P<0.01). Conclusion Daidzein can inhibit oxidative stress and reduce cell apoptosis to antagonize the cardiotoxicity induced by doxorubicin.