title: [The role of mitochondrial K+ channels in the cardioprotection of puerarin against hypoxia/reoxygenation injury in rats].
abstract: OBJECTIVE
  To determine whether the cardioprotection of puerarin (Pue) against hypoxia/reoxygenation injury is mediated by mitochondrial ATP-sensitive potassium channel (mitoK(ATP)) and/or mitochondria calcium-activated potassium channel(mitoK(Ca)).
  
  
  METHODS
  Cardiomyocytes were isolated from male Sprague-Dawley rats and hypoxia/reoxygenation injury was induced by myocyte pelleting model. Cell viability was assessed by trypan blue exclusion and mitochondrial membrane potential was measured by loading with TMRE. 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 hypoxia/reoxygenation injury, while mitochondrial ATP-sensitive potassium channel inhibitor 5-hydroxydecanoate (5-HD, 100 micromol/L, 20 min) or mitochondrial calcium-activated potassium channel blocker paxilline (Pax, 1 micromol/L, 5 min) attenuated the effect of puerarin. The pretreatment with Pue at 0.24 mmol/L for 5 min attenuated collapse of delta-psim induced by hypoxia/reoxygenation injury, 5-HD and Pax abrogated the effect of Pue. In mitochondria isolated from hearts pretreated with Pue, a significant inhibition of Ca(2+)-induced swelling was observed, and this inhibition was attenuated by 5-HD and Pax.
  
  
  CONCLUSIONS
  These findings indicate that Pue protects cardiomyocytes against hypoxia/reoxygenation injury via activating mitoK(ATP) channel and mitoK(Ca) channel, and inhibiting mitochondrial permeability transition pore opening.
authors.affiliation: Hangzhou Normal University School of Basic Medicine, Hangzhou 310036, China.
authors.forename: Hui
authors.initials: H
authors.lastname: Yao
authors.forename: Qin
authors.initials: Q
authors.lastname: Gao
authors.forename: Qiang
authors.initials: Q
authors.lastname: Xia
mesh_terms: D000738:Androsterone / Q000494:pharmacology; D000818:Animals; D015687:Cell Hypoxia / Q000187:drug effects; D002478:Cells, Cultured; D007211:Indoles / Q000494:pharmacology; D007529:Isoflavones / Q000494:pharmacology*; D008297:Male; D033681:Mitochondrial Membrane Transport Proteins / Q000378:metabolism*; D000083162:Mitochondrial Permeability Transition Pore; D009206:Myocardium / Q000166:cytology; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000378:metabolism; D015221:Potassium Channels / Q000378:metabolism*; D024681:Potassium Channels, Calcium-Activated / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D007211:Indoles; D007529:Isoflavones; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D015221:Potassium Channels; D024681:Potassium Channels, Calcium-Activated; C117780:mitochondrial K(ATP) channel; C048220:paxilline; D000738:Androsterone; C033607:puerarin