title: Glutamine decreases intestinal nuclear factor kappa B activity and pro-inflammatory cytokine expression after traumatic brain injury in rats.
abstract: OBJECTIVE
  To investigate whether glutamine supplementation modulates intestinal nuclear factor kappa B (NF-kappaB) activity and pro-inflammatory cytokine expression after traumatic brain injury (TBI) in rats.
  
  
  METHODS
  Right parietal cortical contusion in male rats was made by the weight-dropping method. After trauma, the rats were randomly given chow alone or glutamine mixed chow for 5 d. Gut samples were extracted at 5 d postinjury. We measured NF-kappaB binding activity by electrophoretic mobility shift assay; NF-kappaB subunits p50 and p65 expression by immunohistochemistry; the concentrations of interleukin-1beta, tumor necrosis factor-alpha and interleukin-6 by enzyme-linked immunosorbent assay; intestinal mucosal morphological changes by histopathological study and electron microscopy; and apoptosis by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining.
  
  
  RESULTS
  Administration of glutamine following TBI could decrease NF-kappaB binding activity, NF-kappaB p65 protein expression and concentrations of pro-inflammatory cytokines in the gut. TBI-induced damage of gut structure was ameliorated after glutamine supplementation.
  
  
  CONCLUSIONS
  The results of the present study suggest that the therapeutic benefit of post-TBI glutamine supplementation might be due to its inhibitory effects on intestinal NF-kappaB activation and pro-inflammatory cytokine expression.
authors.affiliation: Department of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, PR China. nju_neurosurgery@163.com
authors.forename: G
authors.initials: G
authors.lastname: Chen
authors.forename: J
authors.initials: J
authors.lastname: Shi
authors.forename: M
authors.initials: M
authors.lastname: Qi
authors.forename: H
authors.initials: H
authors.lastname: Yin
authors.forename: C
authors.initials: C
authors.lastname: Hang
mesh_terms: D000818:Animals; D017209:Apoptosis; D001930:Brain Injuries / Q000378:metabolism*; D002467:Cell Nucleus / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism*; D005786:Gene Expression Regulation; D005973:Glutamine / Q000494:pharmacology*; D053583:Interleukin-1beta / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D007413:Intestinal Mucosa / Q000378:metabolism*; D007422:Intestines / Q000187:drug effects; D008297:Male; D016328:NF-kappa B / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D051996:Transcription Factor RelA / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D016207:Cytokines; D053583:Interleukin-1beta; D015850:Interleukin-6; D016328:NF-kappa B; C498145:Rela protein, rat; D051996:Transcription Factor RelA; D014409:Tumor Necrosis Factor-alpha; D005973:Glutamine