Cardioprotective effects of catalpol against ischemia/reperfusion insult

AIM:To investigate the cardioprotective effect of catalpol in acute myocardial ischemia/reperfusion (MI/R). METHODS: Adult male rats were subjected to 30 min of myocardial ischemia and 3 h of reperfusion and were treated with saline or catalpol (5 mg/kg, i.p., 5 min before reperfusion). Left ventricle systolic pressure (LVSP) and the maximal first derivative of developed pressure (±LV dP/dtmax) were monitored throughout the experiments. Myocardial infarction size, serum creatine kinase (CK) activity, lactate dehydrogenase (LDH) activity, apoptosis index, caspase-3 activity, nitric oxide (NO), superoxide dismutase (SOD), superoxide and peroxynitrite (ONOO-) production were determined at the end of reperfusion. RESULTS: Compared with sham, pretreatment with catalpol significantly improved cardiac functions and reduced myocardial infarction, apoptosis and necrosis of cardiomyocytes after MI/R (all P<0.05). Meanwhile, ONOO- formation was markedly reduced after catalpol treatment (3.01±0.22 vs. 4.66±0.53 pmol/mg protein in vehicle, P<0.05). Catalpol increased NO production and anti-oxidant capacity and reduced MI/R-induced superoxide anion (·O-2) production in I/R hearts. In addition, treatment with the potent ONOO- scavenger uric acid (UA) significantly decreased ONOO- production and protected myocardium against MI/R injury, whereas the same treatment with UA could not further enhance cardioprotective effects of catalpol (P>0.05 vs. catalpol alone). CONCLUSION: Catalpol provides cardioprotection against MI/R insult by attenuating ONOO- formation, which is attributable to the increased NO production and decreased ·O-2 production.