الفهرس 
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Abstract
Gastric ulcer is one of the most common disorders that affect the GIT. It is a major health hazard in terms of both morbidity and mortality. The pathophysiology of gastric ulcer has been considered mainly due to imbalance between harmful factors (acid, pepsin, H. pylori and NSAIDs) and protective factors in the stomach (mucus bicarbonate, blood flow and prostaglandins).
NSAIDs-induced gastric ulcers are the second most common etiology of gastric ulcer. Oral administration of IND, a well-known NSAID, in rats causes ulcerative lesions in the gastric mucosa. IND induces its GIT toxicity via several mechanisms such as generation of pro-inflammatory mediators.
Obestatin is a ghrelin-related peptide. The stomach is the primary site of obestatin expression Obestatin has been reported to be an anorexigenic hormone, decreasing food intake and body weight. Interestingly, obestatin has been reported to have certain effects on GIT including; decrease in gastric emptying time, jejunal motility. Obestatin has been shown to exhibit some protective and therapeutic effects in the gut.
This study was carried out in order to clarify the protective effect of obestatin on acute gastric ulcer induced by IND in adult wistar albino male rats, clarifying the role of VEGF and TNF-α. This study was carried out on 4 main groups of adult wistar albino male rats. The first of them is the control group received a single I.p injection of saline 1 h before a single oral dose of distilled water. The 2nd group received a single I.P injection of obestatin in a dose of (30 μg/kg) 1 h before a single oral dose of distilled water. The 3rdgroup received a single oral dose of IND (40 mg/kg) by orogastric gavage. The 4th group pretreated with a single
I.P injection of obestatin (30μg/kg) 1 h before induction of gastric ulcer by a single oral dose of IND (40 mg/kg) by orogastric gavage. Pyloric ligation was carried out in each animal before IND administration to collect gastric juice.