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Effect of heme oxygenase‐1 induction by octreotide on TNBS‐induced colitis
Author(s) -
Erbil Yeşim,
Giriş Murat,
Abbasoğlu Semra Doğru,
Barbaros Umut,
Yanık Burcu Tulumoğlu,
Necefli Ahmet,
Olgaç Vakur,
Toker Gülçin Aykaç
Publication year - 2007
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/j.1440-1746.2007.04838.x
Subject(s) - medicine , octreotide , ulcerative colitis , heme oxygenase , colitis , glutathione , malondialdehyde , gastroenterology , inflammatory bowel disease , immunohistochemistry , endocrinology , immunology , oxidative stress , heme , biochemistry , chemistry , somatostatin , disease , enzyme
Background and Aim: Ulcerative colitis is a chronic inflammatory disease of the colon and rectum. Although the precise etiology of ulcerative colitis remains unknown, it is believed to involve an abnormal host response to endogenous or environmental antigens, genetic factors, and oxidative damage. The aim of the present study was to investigate whether heme oxygenase‐1 (HO‐1) induction by octreotide could protect against oxidative and inflammatory damage from induced colitis. Methods: Rats received octreotide 50 µg/kg per day intraperitoneally for 5 days before 2,4,6 trinitrobenzene sulfonic acid (TNBS) solution administration and for 15 days following TNBS solution administration. Rats were killed on day 21, and colonic malondialdehyde (MDA) levels, glutathione (GSH) levels and HO‐1 expression were measured. Nuclear factor (NF)‐κB and HO‐1 expression was evaluated by immunohistochemical examination of the colonic tissue. Results: Rats with TNBS‐induced colitis had significantly increased colonic MDA levels and HO‐1 expression in comparison to the control group. Octreotide treatment was associated with increased HO‐1 expression and GSH levels, but decreased MDA levels. Histopathological examination revealed that the intestinal mucosal structure was preserved in the octreotide‐treated group. In addition, treatment with octreotide significantly increased HO‐1 expression and decreased NF‐κB expression by immunohistochemistry when compared to the TNBS‐induced colitis group. Conclusion: Octreotide appears to have protective effects against colonic damage in TNBS‐induced colitis. This protective effect is, in part, mediated by modification of the inflammatory response and the induction of HO‐1 expression.