The effect of heme oxygenase-1 induction by glutamine on TNBS-induced colitis : The effect of glutamine on TNBS colitis

• Published in: International journal of colorectal disease 2007-06, Vol.22 (6), p.591-599
• Main Authors: GIRIS, Murat, ERBIL, Yesim, DOGRU-ABBASOGLU, Semra, YANIK, Burcu Tulumoglu, ALIS, Halil, OLGAC, Vakur, TOKER, Gülcin Aykac
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Caspase 3 - metabolism; Colitis - chemically induced; Colitis - enzymology; Enzyme Induction - drug effects; Gastroenterology. Liver. Pancreas. Abdomen; Glutamine - pharmacology; Glutathione - metabolism; Heme Oxygenase-1 - biosynthesis; Immunohistochemistry; Intestinal Mucosa - drug effects; Intestinal Mucosa - pathology; Male; Malondialdehyde - metabolism; Medical sciences; NF-kappa B - metabolism; Other diseases. Semiology; Rats; Rats, Wistar; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus; Trinitrobenzenesulfonic Acid
• ISSN: 0179-1958; 1432-1262
• DOI: 10.1007/s00384-006-0238-y

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. 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. 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. 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.