Effect of heme oxygenase-1 induction by octreotide on TNBS-induced colitis.
OBJECTIVE
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 microg/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)-kappaB 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-kappaB expression by immunohistochemistry when compared to the TNBS-induced colitis group.


CONCLUSIONS
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.
Erbil
Yeşim
Y
Department of General Surgery, Istanbul Medical Faculty, Istanbul University, Istanbul, Turkey. yerbil2003@yahoo.com
Giriş
Murat
M
Abbasoğlu
Semra Doğru
SD
Barbaros
Umut
U
Yanik
Burcu Tulumoğlu
BT
Necefli
Ahmet
A
Olgaç
Vakur
V
Toker
Gülçin Aykaç
GA
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology* / Q000627:therapeutic use; D000975:Antioxidants / Q000494:pharmacology* / Q000627:therapeutic use; D015153:Blotting, Western; D003093:Colitis, Ulcerative / Q000139:chemically induced / Q000201:enzymology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D003106:Colon / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism / Q000473:pathology; D004195:Disease Models, Animal; D004790:Enzyme Induction / Q000187:drug effects; D005765:Gastrointestinal Agents / Q000494:pharmacology* / Q000627:therapeutic use; D005978:Glutathione / Q000378:metabolism; D006419:Heme Oxygenase (Decyclizing) / Q000096:biosynthesis*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D015282:Octreotide / Q000494:pharmacology* / Q000627:therapeutic use; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D012720:Severity of Illness Index; D013997:Time Factors; D014302:Trinitrobenzenesulfonic Acid
D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D005765:Gastrointestinal Agents; D016328:NF-kappa B; D008315:Malondialdehyde; D014302:Trinitrobenzenesulfonic Acid; D006419:Heme Oxygenase (Decyclizing); C491523:Hmox1 protein, rat; D005978:Glutathione; D015282:Octreotide