title: Using a novel in vivo model to study the function of nuclear factor kappa B in cerebral ischemic injury.
abstract: BACKGROUND
  Cerebral ischemia is a situation with a deficit blood supply to the brain, which eventually leads to cell death, inflammation, and tissue damage. Nuclear factor kappa B (NF-κB) plays an important role in inflammation and immune regulation. The aim of this study was to test the function of the activation of NF-κB in vivo in cerebral ischemic injury.
  
  
  METHODS
  We generated an animal model that used the method of occlusion of the middle cerebral artery (MCAO). The 60 traits were equally divided into 5 groups to investigate the role of NAC pretreatment: (1) sham-operation (control), (2) ischemia for 6 hours, (3) ischemia for 6 hours and NAC pretreatment, (4) ischemia for 24 hours, (5) ischemia for 24 hours and NAC pretreatment. The 36 rats were divided randomly into 3 groups: (A) recombinant adenovirus expressing wild-type κBα(AdIκBαM) group, (B) recombinant adenovirus expressing wild-type IkappaBalpha (AdIκBα) group, and (C) simple ischemia group. Triphenyltetrazolium chloride (TTC) was used to measure infarct volume. Detection of expression of NF-κB was by Immunohistochemistry analysis.
  
  
  RESULTS
  The infarct size of the 24-hours ischemia groups were bigger than those of 6-hours ischemia groups (P<0.01). The infarct size of using NAC pretreatment groups was obviously reduced compared with saline control groups (P<0.01).The percentage of cortical p65-positive cells of the group of (A) were significantly less than the groups of (B) and (C).
  
  
  CONCLUSIONS
  Our data suggest that N-acetylcysteine (NAC) and Ad-IκBα-Mut can inhibit the activation of NF-κB in vivo, reduce the focal infarct size, and protect the brain tissue in ischemia.
authors.affiliation: Department of Neurology, Second Affiliated Hospital of Harbin Medical University, Harbin, China.
authors.forename: Rui
authors.initials: R
authors.lastname: Wang
authors.forename: Songlan
authors.initials: S
authors.lastname: Liang
authors.forename: Hui
authors.initials: H
authors.lastname: Yue
authors.forename: Lijie
authors.initials: L
authors.lastname: Chen
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology / Q000627:therapeutic use; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D002545:Brain Ischemia / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology / Q000517:prevention & control; D004195:Disease Models, Animal; D020672:I-kappa B Proteins / Q000378:metabolism; D008297:Male; D050505:Mutant Proteins / Q000378:metabolism; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D051996:Transcription Factor RelA / Q000378:metabolism
chemical_list: D020672:I-kappa B Proteins; D050505:Mutant Proteins; D016328:NF-kappa B; C000606206:Nfkbia protein, rat; D051996:Transcription Factor RelA; D000072000:NF-KappaB Inhibitor alpha; D000111:Acetylcysteine