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The Protective Effect of Vasoactive Intestinal Peptide (VIP) on Stress‐Induced Gastric Ulceration in Rats
Author(s) -
TUNÇEL NEŞ'E,
ERKASAP N˙ILÜFER,
ŞAH˙INTÜRK VAROL,
AK D˙ILEK DOĞRUKOL,
TUNÇEL MUZAFFER
Publication year - 1998
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1998.tb11191.x
Subject(s) - degranulation , lipid peroxidation , vasoactive intestinal peptide , mast cell , endocrinology , medicine , oxidative stress , chemistry , immunology , receptor , neuropeptide
A bstract : The pathogenesis of cold‐restraint stress ulcer involves various factors and is not completely understood. Mast cell degranulation, increased gastric muscular contractility, diminished mucosal blood flow, release of several biogenic amines, activated polymorphonuclear leukocytes, and lipid peroxidation which results from toxic oxygen molecules were suggested to be related to the production of gastric damage by cold‐restraint stress. Recent evidence strongly indicates that VIP has a modulatory effect on tissue injury. Sprague‐Dawley rats were used in two series of experiments. One set of rats was exposed to cold‐restraint stress with some of the rats pretreated with VIP. The second set of rats was exposed to cold‐restraint stress and then was administered VIP for different durations. Cold‐restraint stress induced gastric lesions and mast cell degranulation and also increased lipid peroxidation in gastric tissue. VIP prevented stress‐induced ulcers and mast cell degranulation and protected gastric tissue from lipid peroxidation. When VIP was used after induction of stress ulcer it was therapeutically beneficial. Thanks to its antioxidant and anti‐inflammatory activity, VIP can be valuable in the prevention of gastric mucosal damage induced by cold‐restraint stress.