Effects of intracerebroventricularly injected glucagon-like peptide-2 on ethanol-induced gastric mucosal damage in rats. (2nd October 2018)

• Record Type: Journal Article
• Authors: Isbil-Buyukcoskun, Naciye; Cam, Betul; Gulec Suyen, Guldal; Ozluk, Kasim
• Is Part Of: Endocrine research. Volume 43:Number 4(2018)
• Page Start: 220
• Page End: 227
• Publication Date: 2018-10-02
• Subjects: Ethanol -- gastric mucosal damage -- glucagon-like peptide-2 -- i.c.v. -- rat; Endocrinology, Experimental -- Periodicals; Endocrinology -- Periodicals; Endocrinology -- Periodicals; Research -- Periodicals; 616.4
• DOI: 10.1080/07435800.2018.1460604
• Languages: English
• ISSNs: 0743-5800

Abstract

ABSTRACT: Purpose : The present study aims to investigate the effects of intracerebroventricularly (i.c.v.)-injected glucagon-like peptide-2 (GLP-2) on ethanol-induced gastric mucosal damage and to reveal the mechanisms involved in this effect. Materials and Methods : Rats received absolute ethanol orally via an orogastric tube 30 minutes after GLP-2 (1–200 ng/10 µl; i.c.v.) or saline (10 µl) injections. They were decapitated 1 hour later, their stomachs were removed, and the gastric mucosal damage was scored. Results : A total of 100 ng GLP-2 inhibited the gastric mucosal damage by 67%. This effect was abolished by the calcitonin gene-related peptide (CGRP) receptor antagonist CGRP-(8-37) (10 µg/kg; s.c.), but was not affected by either the nitric oxide (NO) synthase inhibitor L-NAME (30 mg/kg; s.c.) or the cyclooxygenase inhibitor indomethacin (5 mg/kg; i.p.). The most effective gastroprotective dose of GLP-2 (100 ng/10 µl; i.c.v.), but not the higher doses (150 or 200 ng/10 µl; i.c.v.) prevented the decrease in gastric mucosal blood flow caused by ethanol. In conclusion, i.c.v. GLP-2 protects against ethanol-induced gastric mucosal damage and this effect is mediated by CGRP receptor activation and gastric mucosal blood flow, but not by NO or prostaglandins.