Particularities of Experimental Models Used to Induce Gastric Ulcer

Abstract

Abstract Introduction: Gastric ulcer is one of the most common gastrointestinal diseases, therefore the constant interest for new treatments is due to adverse effects induced by current therapy. The restricted number of in vivo experimental models is a challenge for researchers. Objectives: Identifying the particularities of different types of experimentally induced gastric ulcer in laboratory animals to facilitate their choise for the study of new antiulcer drugs. Material and method: A search in PubMed and Scopus using keywords ( “experimentally” AND “gastric ulcer” AND “rats/mice”) to include experimental studies with the description of local-induced changes. Review articles and in vitro studies were excluded. Results and discussions: Experimental researches on new drugs for gastric ulcer use chemical or surgical methods to induce gastric lesions in rats. Non-steroidal anti-inflammatory drugs (NSAIDs) and acetic acid models to investigate antisecretory and cytoprotective effects; ethanol models evaluate cytoprotective and/or antioxidant effects; pylorus ligature models to evaluate the effects on the secretion of aggressive gastric factors (hydrochloric acid or pepsin). NSAIDs (indomethacin, acetylsalicylic acid or ibuprofen) inhibit cyclooxygenase activity, resulting from reduced mucus and bicarbonate secretion, decreased mucosal blood flow, alteration of microvascular structures, causing epithelial damage Ethanol enhances the proteolytic and hydrolytic action of hydrochloric acid and pepsin; in addition, stimulates the acid secretion and disruptes vascular endothelium. Pylorus ligature determines the accumulation of gastric acid resulting in gastric ulcers due to the autodigestion of the mucosa. Conclusion: The knowledge of the mechanisms to induce experimental gastric ulcers is essential for choosing the model to evaluate new antiulcer agents.