The effect of heme oxygenase-1 induction by glutamine on TNBS-induced colitis |
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Authors: | Murat Giri? Ye?im Erbil Semra Do?ru-Abbaso?lu Burcu Tulumo?lu Yan?k Halil Al?? Vakur Olgaç Gülçin Aykaç Toker |
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Institution: | (1) Department of Biochemistry, Istanbul Medical Faculty, Istanbul University, Capa, Istanbul, Turkey;(2) Department of General Surgery, Istanbul Medical Faculty, Istanbul University, 34340 Capa, Istanbul, Turkey;(3) Oncologic Pathology, Istanbul Medical Faculty, Istanbul University, Capa, Istanbul, Turkey |
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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.
Method 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-κB) and HO-1 expression
were evaluated by immunohistochemical examination of the colonic tissue.
Result 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-κB expression by immunohistochemistry when compared to the TNBS-induced colitis group.
Conclusion 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. |
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Keywords: | TNBS-induced colitis Heme-oxygenase-1 Glutamine Apoptosis |
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