title: [Protective effect of ATP sensitive potassium channel opener on cerebral ischemia/reperfusion injury and its signal transduction mechanism].
abstract: OBJECTIVE
  To study the protective effect of ATP sensitive potassium channel(K( ATP))opener against neuronal apoptosis following focal cerebral ischemia/reperfusion (I/R) and its signal transduction mechanism.
  
  
  METHODS
  Two hundred male Wistar rats were randomly divided into four groups: sham operation group (A group), I/R group (B group), K( ATP) opener treatment group (C group) and K( ATP) opener and blocker treatment group (D group). The middle cerebral artery occlusion (MCAO) by intraluminal suture method was used to reproduce cerebral ischemia, and perfusion was restored 2 hours after MCAO. Five rats in each group were used. Brain sections were made 6, 12, 24, 48 and 72 hours after I/R injury, and neuronal apoptosis was detected by terminal deoxynucleotidyl transferase-mediated deoxyuridine 5 triphosphate nick end labeling (TUNEL). The expressions of caspase-3 and caspase-9 proteins were detected by immunohistochemical method. Another five rats in each group were used for assessing the expressions of caspase-3 mRNA and caspase-9 mRNA by reverse transcription-polymerase chain reaction (RT-PCR).
  
  
  RESULTS
  The number of apoptotic neurons, the expression of caspase-3 and caspase-9 mRNA and protein in B, C and D groups were significantly higher than A group at all time points (P<0.05 or P<0.01). The number of apoptotic neurons, the expressions of caspase-3 and caspase-9 mRNA and protein in C group were significantly lower than B and D groups at all time points (P<0.05 or P<0.01). There were no differences between B and D groups at all time points (all P>0.05).
  
  
  CONCLUSIONS
  K( ATP) opener can significantly mitigate neuronal apoptosis and inhibit the expressions of caspase-3 and caspase-9 mRNA and protein after cerebral I/R injury. This result indicates that K( ATP) opener can decrease neuronal apoptosis by inhibiting mitochondria signaling pathway.
authors: Department of Neurology, The Second Affiliated Hospital of China Medical University, Shenyang, Liaoning, China.
authors: Hong
authors: H
authors: Zhang
authors: Yan-Yan
authors: YY
authors: Liu
authors: Ying
authors: Y
authors: Ma
authors: Yong-Li
authors: YL
authors: Lu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D001921:Brain / Q000473:pathology; D002545:Brain Ischemia / Q000378:metabolism* / Q000473:pathology / Q000517:prevention & control; D053148:Caspase 3 / Q000378:metabolism; D053453:Caspase 9 / Q000378:metabolism; D004195:Disease Models, Animal; D020244:Infarction, Middle Cerebral Artery / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control; D008297:Male; D015221:Potassium Channels / Q000819:agonists*; D012333:RNA, Messenger / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000378:metabolism* / Q000473:pathology / Q000517:prevention & control; D015398:Signal Transduction
chemical_list: D015221:Potassium Channels; D012333:RNA, Messenger; D053148:Caspase 3; D053453:Caspase 9