title: [Role of protein kinase C in protecting rats against pulmonary ischemia reperfusion injury through opening of mitochondrial ATP sensitive potassium channel].
abstract: OBJECTIVE
  To investigate the effect of opening of mitochondrial ATP-sensitive potassium channel on inducing lung protection against ischemia reperfusion injury (I/R) and the role of PKC in the protective effect.
  
  
  METHODS
  Fifty-six rats were divided into six groups, including sham-operation group, I/R group, DE (diazoxide) +I/R group, 5-HD (5-hydroxydecanoic acid) +DE+I/R group, CHE (chelerythrine) +DE+I/R group and 5-HD +PMA (phorbol 12-myristate 13-acetate)+ I/R group. Pulmonary I/R injury rat models were established by 45 min of left hilar clipping followed by 180 min of reperfusion. Morphological changes in lung tissues were detected by HE staining. The wet-to-dry weight ratio of lung tissues was evaluated. Cytochrome C expression in lung tissues was assessed by immunohistochemical staining. TUNEL was used to determine apoptosis. Protein kinase C (PKC) activity in lung tissues was assessed by PepTag non-radioactive assay.
  
  
  RESULTS
  Compared with I/R group, the lung tissue morphology of the rats in the DE+I/R group was preserved well and the wet-to-dry weight ratio, expression of cytochrome C and apoptosis index decreased significantly (P < 0.05). The PKC activity in the lung tissues of the rats in the DE+ I/R group increased dramatically. Both pretreatment with 5-HD and CHE blocked the protective effect induced by DE preconditioning. There were no differences between 5-HD+PMA+I/R group and I/R group in the above indicators except for PKC activation. These results showed that blocking of mitochondrial ATP-sensitive potassium channel by 5-HD did not protect lung from ischemia reperfusion injury even though PKC were activated.
  
  
  CONCLUSIONS
  Opening of mitochondrial ATP-sensitive potassium channel plays an essential protective role in pulmonary ischemia reperfusion injury. The pulmonary protection appears to be dependent on PKC activation.
authors.affiliation: Department of Pathophysiology, Guiyang Medical College, Guiyang 550004, China.
authors.forename: De-Qin
authors.initials: DQ
authors.lastname: Lu
authors.forename: Ying
authors.initials: Y
authors.lastname: Chen
authors.forename: Tao
authors.initials: T
authors.lastname: Li
authors.forename: Bao-Luo
authors.initials: BL
authors.lastname: Li
mesh_terms: D000818:Animals; D053119:Benzophenanthridines / Q000494:pharmacology; D005260:Female; D054086:KATP Channels / Q000187:drug effects / Q000502:physiology*; D008168:Lung / Q000098:blood supply*; D008297:Male; D008928:Mitochondria / Q000378:metabolism*; D011493:Protein Kinase C / Q000037:antagonists & inhibitors / Q000378:metabolism*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000517:prevention & control*; D013755:Tetradecanoylphorbol Acetate / Q000031:analogs & derivatives / Q000494:pharmacology
chemical_list: D053119:Benzophenanthridines; D054086:KATP Channels; C020922:4-O-methyl-12-O-tetradecanoylphorbol 13-acetate; C016299:chelerythrine; D011493:Protein Kinase C; D013755:Tetradecanoylphorbol Acetate