The use of animal models to study the cause and cure for gastrointestinal mucosal injury has been pursued since the time of Pavlov through different methods. Fundamentally, there are natural causes like the incompetence of the pyloric sphincter allowing the duodenal contents to reflux into the stomach, delayed gastric emptying due to antral hypomotility, and the position and movement of muscle bands in the stomach, all contributing towards the production of gastritis and predispose to ulceration. Psychological stress and anxiety are associated with gastrointestinal dysfunction leading to gastric hyper-acid secretion and haemorrhagic lesions. Generation of reactive oxygen species (ROS) in tissues can lead to damage of cellular metabolic systems and subsequently, cause inflammation by initiation of lipid peroxidation reactions. Recent studies have brought new insight into the activities of Helicobacter pylori colonization in the stomach, leading to the pathogenesis of not only autoimmune and inflammatory diseases, but also apoptosis. This review discusses the pathogenesis of gastroduodenal erosions and how they are eradicated through suppression of the causes and the mechanisms involved. The mechanisms behind the protective effect of certain group of drugs like histamine H2 receptor antagonists, proton pump inhibitors, growth factors and peptides, centrally active drugs and their molecular pathways of cellular activation are discussed in this review. The influence of prostaglandins, nitric oxide, bicarbonate, mucus, as well as cell restitution and proliferation on the epithelial cells, are delineated. In future, a combination of these biochemical and genetic approaches will bring a detailed understanding of the physiology and pathology of the gastrointestinal remedial system.
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