Coptisine exert cardioprotective effect through anti-oxidative and inhibition of RhoA/Rho kinase pathway on isoproterenol-induced myocardial infarction in rats

ObjectiveBecause myocardial infarction is a major cause of morbidity and mortality worldwide, protecting the heart from the ischemia is the focus of intense research. Coptisine is an isoquinoline alkaloid extracted form Coptidis Rhizoma. This study aims to elucidate if coptisine is responsible for cardioprotection using myocardial infarction (MI) rat models and investigate its potential mechanism of action.MethodsMyocardial infarction was produced in rats with 85 mg kg−1 isoproterenol administered subcutaneously twice at an interval of 24 h. The rats were randomized into 7 groups: (I) Normal; (II) ISO; (III) ISO + fasudil; (IV) ISO + isosorbide dinitrate (ISDN) and (V-VII) ISO + coptisine (25, 50 and 100 mg kg−1). Cardiac function and markers of cardiac ischemic were assessed after MI.ResultsRats pretreated with coptisine (25, 50 and 100 mg kg−1) for 21 days and received subcutaneously injected with ISO (85 mg kg−1) on the 20th and 21st day at an interval of 24 h. The results suggested that coptisine has strong antioxidant activity, and it can maintain cell membrane integrity, ameliorate mitochondrial respiratory dysfunction, reduce myocardial cells apoptosis, inhibit RhoA/ROCK expression induced by high-dose isoproterenol administration.ConclusionsCoptisine provided cardioprotection in a model of myocardial infarction, and therefore should be considered as a novel adjunctive therapy for attenuating myocardial damage.

► Using isoproterenol induced myocardial infarction rat models to elucidate the effect of coptisine and investigate its potential mechanism. ► Coptisine has strong antioxidant activity. ► Coptisine significantly inhibit RhoA/ROCK expression induced by isoproterenol.