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  • Title: Improvement of ventricular mechanical properties by puerarin involves mitochondrial permeability transition in isolated rat heart during ischemia and reperfusion.
    Author: Gao Q, Pan HY, Bruce IC, Xia Q.
    Journal: Conf Proc IEEE Eng Med Biol Soc; 2005; 2005():5591-4. PubMed ID: 17281523.
    Abstract:
    The aim of the present study was to determine whether the clinically effective cardioprotection conferred by puerarin (Pue) against ischemia and reperfusion is mediated by mitochondrial transmembrane pores and/or channels. In isolated rat hearts subjected to 30 min regional ischemia and 120 min reperfusion, pretreatment with Pue at 0.24 mmol/L for 5 min before ischemia increased myocardial formazan content, an index of myocardial viability, reduced lactate dehydrogenase release, improved recovery of the 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) during reperfusion. Administration of atractyloside (20 micromol/L), an opener of the mitochondrial permeability transition pore, for the first 20 min of reperfusion and 5-hydroxydecanoate (100 micromol/L), the mitochondrial specific ATP-sensitive potassium channel blocker, for 20 min before ischemia, attenuated the protective effects of Pue. In mitochondria isolated from hearts pretreated with 0.24 mmol/L Pue for 5 min, a significant inhibition of Ca2+-induced swelling was observed, and this inhibition was attenuated by 5-hydroxydecanoate. These findings indicate that Pue protects the myocardium against ischemia and reperfusion injury via inhibiting mitochondrial permeability transition pore opening and activating the mitochondrial ATP-sensitive potassium channel.
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