Loading…

Effect of orexin-a on ischemia-reperfusion-induced gastric damage in rats

Background Orexins are involved in the regulation of sleeping behavior and energy homeostasis, and they are also implicated in the regulation of gastrointestinal functions. Previous reports have demonstrated the expression of orexin receptors in the gastrointestinal system. The aim of this study was...

Full description

Saved in:
Bibliographic Details
Published in:Journal of gastroenterology 2008-03, Vol.43 (3), p.202-207
Main Authors: Bülbül, Mehmet, Tan, Ruken, Gemici, Burcu, Öngüt, Gözde, İzgüt-Uysal, V. Nimet
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Background Orexins are involved in the regulation of sleeping behavior and energy homeostasis, and they are also implicated in the regulation of gastrointestinal functions. Previous reports have demonstrated the expression of orexin receptors in the gastrointestinal system. The aim of this study was to investigate the gastroprotective effect of orexin-A in ischemia-reperfusion-induced gastric mucosal injury. Methods The gastric ischemia-reperfusion model was established by clamping the celiac artery for 30 min and reperfusing for 60 min. Orexin-A was administered in doses of 500 pmol·kg −1 ·min −1 by infusion throughout the ischemia-reperfusion period. The mean lesion area, gastric prostaglandin E 2 and mucus content, myeloperoxidase activity, and production of thiobarbituric acid reactive substances were measured. Results Orexin-A significantly attenuated the ischemia-reperfusion-induced gastric lesions and also decreased myeloperoxidase activity and the thiobarbituric acid reactive substances content in gastric mucosa of rats exposed to ischemia-reperfusion. However, the decline in gastric prostaglandin E 2 and mucus content was not restored by orexin-A treatment. Conclusions Orexin-A exhibited a gastroprotective effect against ischemia-reperfusion-induced lesions by decreasing neutrophil activation and lipid peroxidation.
ISSN:0944-1174
1435-5922
DOI:10.1007/s00535-007-2148-3