title: The effect of heme oxygenase-1 induction by glutamine on TNBS-induced colitis. The effect of glutamine on TNBS colitis.
abstract: BACKGROUND
  Inflammatory bowel disease is a multifactorial inflammatory disease of the colon and rectum with an unknown etiology. In the present study, we aimed to investigate whether heme oxygenase-1 (HO-1) induction by glutamine could protect colitis-induced damage from oxidative, inflammatory, and apoptotic damage.
  
  
  METHODS
  The rats were divided into four groups. Group 1 had TNBS colitis alone, group 2 had TNBS-induced colitis and glutamine 1 g/kg/day intragastric gavage for 3 days before TNBS solution administration and 15 days following TNBS solution administration, group 3 had glutamine alone 1 g/kg/day intragastric gavage for 18 days before being killed, and group 4 had isotonic saline solution alone 1 cm3/rat intragastric gavage for 18 days before being killed. Colonic malondialdehyde (MDA) levels, glutathione (GSH) levels, caspase-3 activities, and HO-1 expressions of the killed rats were measured. Nuclear factor kappa B (NF-kappaB) and HO-1 expression were evaluated by immunohistochemical examination of the colonic tissue.
  
  
  RESULTS
  TNBS-induced colitis significantly increased the colonic MDA levels, caspase-3 activities, and HO-1 expression in comparison to the control group. Glutamine treatment was associated with increased HO-1 expression and GSH levels and decreased MDA levels and caspase-3 activity. Histopathological examination revealed that the intestinal mucosal structure was preserved in the glutamine-treated group. In addition to this, treatment with glutamine significantly increased HO-1 expression and decreased NF-kappaB expression by immunohistochemistry when compared to the TNBS-induced colitis group.
  
  
  CONCLUSIONS
  Glutamine reduced colonic damage in TNBS-induced colitis. The mechanism of the protection associated with glutamine was due to antioxidant, antiapoptotic, anti-inflammatory, and HO-1 induction effects.
authors.affiliation: Department of Biochemistry, Istanbul Medical Faculty, Istanbul University, Capa, Istanbul, Turkey.
authors.forename: Murat
authors.initials: M
authors.lastname: Giriş
authors.forename: Yeşim
authors.initials: Y
authors.lastname: Erbil
authors.forename: Semra
authors.initials: S
authors.lastname: Doğru-Abbasoğlu
authors.forename: Burcu Tulumoğlu
authors.initials: BT
authors.lastname: Yanik
authors.forename: Halil
authors.initials: H
authors.lastname: Aliş
authors.forename: Vakur
authors.initials: V
authors.lastname: Olgaç
authors.forename: Gülçin Aykaç
authors.initials: GA
authors.lastname: Toker
mesh_terms: D000818:Animals; D053148:Caspase 3 / Q000378:metabolism; D003092:Colitis / Q000139:chemically induced / Q000201:enzymology*; D004790:Enzyme Induction / Q000187:drug effects; D005973:Glutamine / Q000494:pharmacology*; D005978:Glutathione / Q000378:metabolism; D051547:Heme Oxygenase-1 / Q000096:biosynthesis*; D007150:Immunohistochemistry; D007413:Intestinal Mucosa / Q000187:drug effects / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D014302:Trinitrobenzenesulfonic Acid
chemical_list: D016328:NF-kappa B; D005973:Glutamine; D008315:Malondialdehyde; D014302:Trinitrobenzenesulfonic Acid; D051547:Heme Oxygenase-1; D053148:Caspase 3; D005978:Glutathione