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AIM Coptisine is an isoquinoline alkaloid extracted from Coptidis Rhizoma.This study aims to elucidate if coptisine is responsible for cardioprotection using myocardial infarction (MI) and investigate its mechanism.METHODS Rats were randomized into 7 groups: normal, isoproterenol (Iso), Iso + fasudil, Iso + isosorbide dinitrate and Iso + coptisine (25, 50, 100 mg· kg-1).Rats pretreated with coptisine for 21 d (ig) and injected subcutaneously with high-dose Iso (85 rag· kg-1) on the 20th, 21st day at an interval of 24 h.Cardiac function and biomarkers of cardiac ischemia were assessed after MI.RESULTS Coptisine has strong antioxidant activity, and it can maintain cell membrane integrity, ameliorate mitochondrial respiratory dysfunction, reduce myocardial cells apoptosis, inhibit RhoA/ROCK expression in experimental MI rats.CONCLUSION The present study provides experimental evidence that coptisine has strong antioxidant activity, and it can maintain cell membrane integrity, ameliorate mitochondrial respiratory dysfunction and improve cardiac systolic/diastolic dysfunction induced by Iso.Inhibition of RhoA/ROCK pathway was involved in coptisine induced cardioprotection effects on experimental MI.Coptisine should be considered as a novel adjunctive therapy for attenuating myocardial damage.