DEVELOPMENT AND ASSESSMENT OF A CHRONIC ATROPHIC GASTRITIS ANIMAL MODEL REFLECTING GASTRIC YIN DEFICIENCY FOR SPORTS HEALTH RESEARCH

Abstract

Objective: To develop and validate an integrated disease and syndrome model of chronic atrophic gastritis (CAG) in rats, simulating gastric yin deficiency conditions. Methods: The model involved administering a combination of ranitidine hydrochloride in feed and N-methyl-N-nitro-N-nitrosoguanidine (MNNG) in drinking water, supplemented by alternate gavage with heated saline and ethanol, alongside controlled feeding cycles to induce hunger and satiety fluctuations. Histopathological evaluations of gastric mucosa were conducted using hematoxylin and eosin staining, while transmission electron microscopy assessed cellular ultrastructural changes. Serum gastric function parameters were measured via enzyme-linked immunoassays, gastric acid levels via pH metrics, and overall physiological responses were monitored through a set of validated biomarkers. Results: After 10 weeks, significant morphological changes in gastric tissues were observed, including mucosal thinning and glandular depletion. Electron microscopy highlighted cellular atrophy and structural disruptions, such as decreased pepsinogen granules and mitochondrial damage. Serum analysis indicated a reduction in gastric function markers and an increase in gastric pH, corroborating gastric dysfunction. Physiological observations included weight loss, decreased food intake, altered stool moisture, and heightened pain response, aligning with the symptoms of gastric yin deficiency. Conclusion: The combined use of MNNG, ranitidine, thermal gavage treatments, and dietary manipulations effectively established a rat model of CAG mimicking gastric yin deficiency. This model replicates the human condition's pathophysiological features, providing a valuable tool for future research into the mechanisms and treatments of gastric yin deficiency and CAG.