title: Sevoflurane and isoflurane preconditioning provides neuroprotection by inhibition of apoptosis-related mRNA expression in a rat model of focal cerebral ischemia.
abstract: BACKGROUND
  This study aimed to examine the effects of sevoflurane or isoflurane preconditioning on cerebral ischemia/reperfusion-induced inflammation, oxidative stress, and lipid peroxidation and test the hypothesis that the underlining mechanism of the protective effect of preconditioning involves changes in the apoptotic gene expression profiles in an experimental model of middle cerebral artery occlusion in rats.
  
  
  METHODS
  Twenty-four adult male rats were randomly divided into 3 groups: control (n=8), sevoflurane (n=8), and isoflurane (n=8). For preconditioning, these 3 groups were exposed to 40% O2, 2% sevoflurane, and 1.5% isoflurane, respectively, for 60 minutes, followed immediately by 1 hour of middle cerebral artery occlusion and then 6 hours of reperfusion. Blood and brain tissue samples were collected for determination of blood gas tension, tumor necrosis factor-α, interleukin-6, and interleukin-1β. Brain tissue samples were collected for determination of the wet/dry ratio, myeloperoxidase, malondialdehyde, and total RNA and also for histologic examinations.
  
  
  RESULTS
  Tumor necrosis factor-α, interleukin-1β, and myeloperoxidase levels decreased and antioxidant enzyme levels increased in the sevoflurane group compared with the control and isoflurane groups. Proapoptotic genes (Tnf, Tnfrsf10b, and Tp53) downregulated and antiapoptotic genes (Aven, Bcl2, Bcl2l2, and Prok2) upregulated with sevoflurane treatment compared with the isoflurane and control groups. Both isoflurane and sevoflurane pretreatment decreased malondialdehyde, Dffb, the wet/dry ratio, and injury score and upregulated Bax and Apaf 1 compared with the control group.
  
  
  CONCLUSIONS
  Sevoflurane and isoflurane preconditioning ameliorates inflammation, cerebral lipid peroxidation, and histologic injury. Downregulation of proapoptotic molecules and upregulation of antiapoptotic molecules may be associated with this effect.
authors.affiliation: Department of Anesthesiology, Gazi University Medical School, Ankara, Turkey. nurbedirli@yahoo.com
authors.forename: Nurdan
authors.initials: N
authors.lastname: Bedirli
authors.forename: Emin Umit
authors.initials: EU
authors.lastname: Bagriacik
authors.forename: Hakan
authors.initials: H
authors.lastname: Emmez
authors.forename: Guldal
authors.initials: G
authors.lastname: Yilmaz
authors.forename: Yusuf
authors.initials: Y
authors.lastname: Unal
authors.forename: Zerrin
authors.initials: Z
authors.lastname: Ozkose
mesh_terms: D018685:Anesthetics, Inhalation / Q000494:pharmacology*; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D017209:Apoptosis / Q000187:drug effects*; D051017:Apoptosis Regulatory Proteins / Q000096:biosynthesis*; D001929:Brain Edema / Q000378:metabolism; D002560:Cerebrovascular Circulation / Q000187:drug effects; D016207:Cytokines / Q000097:blood; D020244:Infarction, Middle Cerebral Artery / Q000150:complications; D002546:Ischemic Attack, Transient / Q000188:drug therapy* / Q000473:pathology; D007530:Isoflurane / Q000494:pharmacology*; D008297:Male; D008738:Methyl Ethers / Q000494:pharmacology*; D018696:Neuroprotective Agents; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D017208:Rats, Wistar; D000077149:Sevoflurane
chemical_list: D018685:Anesthetics, Inhalation; D000975:Antioxidants; D051017:Apoptosis Regulatory Proteins; D016207:Cytokines; D008738:Methyl Ethers; D018696:Neuroprotective Agents; D012333:RNA, Messenger; D000077149:Sevoflurane; D007530:Isoflurane