【Abstract】 Objective To investigate the protective effect and mechanism of deferiprone on alcohol-induced myocardial injury. Methods Twenty-four 7-week-old male C57/BL6J mice were randomly divided into control group, model group and deferiprone treatment group after one week of adaptive feeding, with 8 mice in each group. Alcoholic myocardial injury model was established by gavage of 50% alcohol (10 mL·kg-1) at 17 o "clock every day. The model group and deferiprone intervention group were given 50% alcohol (10 mL· kg-1) by gavage at the same time every day, and the control group was given the same dose of normal saline. One hour later, the deferiprone intervention group was given deferiprone solution (100 mg·kg-1 ·d) by gavage, and the control group and the model group were given the same dose of normal saline. 12 weeks later, cardiac tissues and blood were taken from the groups, and pathological changes in cardiac tissues were observed with H E staining, and serum and cardiac tissues of the mice were tested for lactate dehydrogenase (LDH). Lactate dehydrogenase (LDH) level and Fe2+ content were detected, and myocardial tissue malondialdehyde (MDA) content was detected.? ?? Results? Compared with the control group, myocardial fibres in the model group were fractured and lysed, the extracellular space was significantly widened, and inflammatory cells were infiltrated; serum and myocardial tissue LDH levels and Fe2+ content were elevated; and myocardial MDA content was significantly increased in the model group compared with that in the control group (P＜0.05). After the intervention of deferiprone, myocardial fibre fracture, lysis and extracellular gap were significantly improved, and a small amount of inflammatory cell infiltration; the level of serum, myocardial tissue LDH and Fe2+ content and myocardial MDA content were significantly reduced compared with the model group (P＜0.05). Conclusion Deferiprone has a protective effect on mice with alcoholic myocardial injury, and its mechanism may be related to the inhibition of cardiomyocyte iron overload and the reduction of oxidative stress damage by alcohol.