Abstract: AIM: To investigate the protective effects and mechanisms of methylflavonolamine (MFA)on myocardial injury induced by adriamycin in mice.METHODS: The myocardial injury was induced by Adriamycin (ADR)1.5 mg·kg^-1 ip once every two days for ten days in mice.All mice were taken the electrocardiogram examination before given drugs.The mice with abnormal electrocardiogram were excluded prior to the experiment.The degree of J point elevation, the prolonged degree of the QRS complex duration and the Q-T interval, the change of contents of serum creatine phosphokinase (CK), serum lactate dehydrogenase (LDH), myocardial malondialdehyde (MDA), and the activity of myocardial superoxide dismutase (SOD)were observed in control and treated groups. The contents of serum CK and LDH were measured by spectrophotometry, and the content of myocardial MDA was measured by TBA method and the activity of myocardial SOD by hydroxylamine method.RESULTS: The J point was elevated, the Q-T interval and the duration of QRS complex were prolonged and the contents of serum CK and LDH were increased in mice with acute myocardial injury induced by ADR, suggesting that a widespread and severe myocardial cell injury occurred in the prepared models. While all these injury indices were reversed by MFA treatment. The content of myocardial MDA was increased and the activity of myocardial SOD was decreased in mice with myocardial injury, and MFA decreased the MDA content and increased the SOD activity, indicating that it possesses the actions of scavenging free oxygen radicals and anti-lipoperoxidation.CONCLUSIONS: MFA significantly alleviates the degree of the acute myocardial injury in mice induced by ADR. Its mechanism may be associated with reducing oxygen free radical production and anti-lipoperoxidation.

Key words: methylflavonolamine, adriamycin, superoxide dismutase, malondialdehyde, oxygen free radicals, myocardial injury