Benidipine prevents oxidative stress, inflammatory changes and apoptosis related myofibril damage in isoproterenol-induced myocardial infarction in rats

OBJECTIVE: The effects of benidipine on oxidative stress and myocardial apoptosis were assessed in isoproterenol (ISO)-induced myocardial infarction (MI) in wistar rats. MATERIALS AND METHOD: Animals were pretreated with benidipine (1, 3, 10 μg/kg/day Body weight) intravenously for a period of 28 days. After pretreatment, ISO (85 mg/kg Body weight, subcutaneous) was injected in rats at an interval of 24 h to induce MI. Myocardial oxidative stress, cardiac biomarkers, apoptosis, inflammatory mediators, and ultrastructural architecture of the cardiac tissue were assessed in ISO-induced MI in rats. RESULT: Significant variation in the level of TBA, antioxidant enzymes (GSH, CAT, SOD, GPx, GRx, GST) in myocardium, cardiac biomarkers (CK-MB, LDH) in serum, Caspase-3, C-reactive protein (CRP), and alteration in ultrastructural architecture of cardiac tissue confirmed the cardiotoxicity induced by ISO. Pretreatment with benidipine preserved the lipid peroxide and antioxidant enzymes, and furthermore showed maintained levels of myocardial biomarker, CRP and caspase-3. Ultrastructure architecture of cardiac tissue was also found to be well preserved. CONCLUSION: The present study suggested cardioprotective effect of benidipine which may possibly be due to its antioxidant activity and antiapoptotic nature.