title: [Sevoflurane preconditioning induced delayed neuroprotection against focal cerebral ischemia in rats].
abstract: OBJECTIVE
  To investigate whether the reactive oxygen species (ROS) and mitochondrial ATP-sensitive potassium (mitoKATP) channels were involved in delayed neuroprotection induced by sevoflurane on tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) levels.
  
  
  METHODS
  Eighty-four male SD rats weighing 250 approximately 280 g, undergoing thread embolism of the right middle cerebral artery occlusion (MCAO) to cause focal ischemia for 2 h and then undergoing 24 h reperfusion, were randomly divided into 7 groups (n=12, each): a sham group(S), an ischemia-reperfusion group (I/R), a sevoflurane preconditioning group (Sevo), a 2-mercaptopropionylglycine (ROS scavenger)+sevoflurane group (MPG+Sevo), a 5-hydroxydecanoate (a mitoK(ATP) blocker) + sevoflurane group (5-HD+Sevo), an MPG group, and a 5-HD group. The protein level of TNF-alpha and IL-1beta in the cerebral issue was detected by enzyme linked immunosorbent assay (ELISA) and the expression of mRNA was measured by semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR).
  
  
  RESULTS
  Apoptosis index (AI), the protein level and the mRNA expression of TNF-alpha and IL-1beta were significantly higher in the I/R group than those of Group S. Pre-administration of sevoflurane could inhibit the increase of the protein level and the expression of mRNA of TNF-alpha, and IL-1beta and attenuate the cerebral damage induced by ischemia-reperfusion. Neuroprotection of sevoflurane preconditioning was abolished by MPG and 5-HD. However, MPG and 5-HD alone had no effect.
  
  
  CONCLUSIONS
  Sevoflurane can produce delayed protection against cerebral ischemia-reperfusion injury by down-regulating TNF-alpha, IL-1beta protein, and mRNA expression.
authors.affiliation: Department of Anesthesia, Central South University, Changsha 410078, China.
authors.forename: Zhi
authors.initials: Z
authors.lastname: Ye
authors.forename: Qulian
authors.initials: Q
authors.lastname: Guo
authors.forename: E
authors.initials: E
authors.lastname: Wang
authors.forename: Min
authors.initials: M
authors.lastname: Shi
authors.forename: Yundan
authors.initials: Y
authors.lastname: Pan
mesh_terms: D000818:Animals; D020925:Hypoxia-Ischemia, Brain / Q000150:complications / Q000188:drug therapy*; D020244:Infarction, Middle Cerebral Artery / Q000150:complications / Q000188:drug therapy; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D019194:Ischemic Preconditioning / Q000379:methods*; D054086:KATP Channels / Q000378:metabolism; D008297:Male; D008738:Methyl Ethers / Q000494:pharmacology / Q000627:therapeutic use*; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D015427:Reperfusion Injury / Q000209:etiology / Q000517:prevention & control*; D000077149:Sevoflurane; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D053583:Interleukin-1beta; D054086:KATP Channels; D008738:Methyl Ethers; D018696:Neuroprotective Agents; D012333:RNA, Messenger; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D000077149:Sevoflurane