title: [Mitochondrial mechanism of cardioprotective effect of puerarin against H202-stress in rats].
abstract: OBJECTIVE
  To determine whether the cardioprotection of puerarin (Pue) against H202-stress is mediated by mitochondrial transmembrane pores and/or channels.
  
  
  METHODS
  Cardiomyocytes were isolated from male Sprague-Dawley rats. Cell viability was assessed by trypan blue exclusion and mitochondrial membrane potential was measured by loading with Rhodamine 123. The opening of mitochondrial permeability transition pore was determined spectrophotometrically.
  
  
  RESULTS
  Pretreatment with Pue at 0.24 mmol/ L for 5 min increased the cell viability against H2O2-stress, while mitochondrial calcium-activated potassium channel blocker paxilline (Pax, 1 micromol/L, 5 min) or PKC inhibitor(chelerythrine, 5 micromol/L, 30 min) attenuated the effect of puerarin. The pretreatment with Pue at 0.24 mmol/L for 5 min or mitochondrial calcium-activated potassium channel opener NS 1619 (10 micromol/L, 10 min) attenuated mitochondrial depolarization induced by H2O2-stress, while mitochondrial permeability transition pore opener atractyloside (20 micromol/L, 20 min) abrogated the effect of Pue. In mitochondrial isolated from hearts pretreated with 0.24 mmol/L Pue for 5 min, a significant inhibition of Ca2+ -induced swelling was observed, which inhibition was attenuated by Pax (1 micromol/L, 5 min).
  
  
  CONCLUSIONS
  These findings indicate that Pue protects cardiomyocytes against H2O2-stress via inhibiting mitochondrial permeability transition pore opening and activating mitochondrial calcium-activated potassium channel.
authors.affiliation: Department of Physiology, Zhejiang University School of Medicine, Hangzhou 310058, China.
authors.forename: Bo
authors.initials: B
authors.lastname: Yang
authors.forename: Qin
authors.initials: Q
authors.lastname: Gao
authors.forename: Hui
authors.initials: H
authors.lastname: Yao
authors.forename: Qiang
authors.initials: Q
authors.lastname: Xia
mesh_terms: D000818:Animals; D002316:Cardiotonic Agents / Q000494:pharmacology*; D002469:Cell Separation; D002470:Cell Survival / Q000187:drug effects; D006861:Hydrogen Peroxide; D007529:Isoflavones / Q000494:pharmacology*; D008297:Male; D053078:Membrane Potential, Mitochondrial / Q000502:physiology*; D008929:Mitochondria, Heart / Q000502:physiology*; D033681:Mitochondrial Membrane Transport Proteins / Q000037:antagonists & inhibitors; D000083162:Mitochondrial Permeability Transition Pore; D032383:Myocytes, Cardiac / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D024681:Potassium Channels, Calcium-Activated / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013312:Stress, Physiological
chemical_list: D002316:Cardiotonic Agents; D007529:Isoflavones; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D024681:Potassium Channels, Calcium-Activated; D006861:Hydrogen Peroxide; C033607:puerarin