AIMTo determine whether the cardioprotection of puerarin (Pue) against ischemia/reperfusion (I/R) is mediated by mitochondrial transmembrane pore or channels.

METHODSMale Sprague-Dawley rats were used for Langendorff isolated heart perfusion. The hearts subjected to global ischemia for 30 min followed by 120 min of reperfusion. Formazan, a product of 2,3,5-triphenyltetrazolium chloride (TTC), which is proportional to myocardial viability, was measured at 490 nm, and the level of lactate dehydrogenase (LDH) in the coronary effluent was measured to evaluate the cardiac injury.

RESULTSThe pretreatment with Pue at 0.24 mmol/L for 5 min before ischemia increased formazan content of myocardium, reduced LDH release, improved the recovery of the left ventricular developed pressure, maximal rise/fall rate of left ventricular pressure, left ventricular end-diastolic pressure and rate pressure product (left ventricular developed pressure multiplied by heart rate) and attenuated the decrease of coronary flow during reperfusion. Administration of atractyloside (20 micromol/L), an opener of mitochondrial permeability transition pore, for 20 min (first 20 min of reperfusion) and 5-hydroxydecanoate (100 micromol/L), the mitochondrial specific K(ATP) blocker, for 20 min before ischemia attenuated the protective effects of Pue.

CONCLUSIONThe findings indicate that in the isolated rat heart, Pue protects myocardium against ischemia/ reperfusion injury via the opening of mitochondrial ATP-sensitive potassium channel and the inhibition of mitochondrial permeability transition pore opening.