动物模型,慢性萎缩性胃炎 z-bo 2020-08-07 438

　　(1) Reproduction method Adult rats, orally give 15% sodium chloride (NaCl) solution at 55℃ or simply give 10ml/kg body weight of distilled water at 55℃ once a day for 12 to 32 weeks. During the continuous observation of the general activity of the animal, after modeling, anesthetize the abdomen and take the stomach, cut along the greater curve for general observation, including the color, elasticity, folds, and mucus of the mucous membrane, and quickly take the material along the minor curve, including the stomach The antrum and part of the gastric body are then examined by histopathology. The standards for chronic atrophic gastritis were established in accordance with the 1994 Houston gastritis diagnostic classification standard and the 2000 Jinggangshan gastritis classification standard, and the mucosal thickness, gland width and cell thickness were measured with a micrometer.

　　(2) Model features 15% NaCl hot water solution was administered to the stomach for 2 weeks. A small amount of eosinophils and lymphocytes began to infiltrate between the gastric mucosal muscle layer and the mucosal layer. The amount increased at 4 weeks, and the mucosal glands became narrow at 6 weeks. The distance between the muscularis mucosa and the glands is widened, and there are more lymphocytes and fibroblasts proliferating in between. The proliferating fibroblasts are parallel to the mucosal glands, and the eosinophils are reduced. At 8 weeks, the proliferation of fibroblasts is obvious. The smooth muscle of the muscularis mucosa is inserted into the lamina propria in a spike-like shape, the blood vessels are dilated and congested, and a small amount of lymphocytes and eosinophils are infiltrated. At 10 to 12 weeks, the gastric mucosal glands are significantly reduced, and the smooth muscles of the muscularis mucosa are proliferating in bundles. Inserted into the lamina propria of the mucosa, the glandular epithelium of the upper 1/3 to 2/3 of the gland atrophies, the glandular lumen widens, and the width of the gastric pit neck mucosa narrows. At this time, electron microscopy showed that the surface of the gastric mucosal cells of the model animals was rough, the mucosal surface was eroded and flat. At 32 weeks, the gastric mucosal cells were atrophy, the diameter of the glandular cavity increased, the cell surface was broken, and there was fibrous exudation. After gavage with hot water alone to 24 weeks, the gastric mucosal glands are significantly reduced, and the upper 1/3 to 2/3 of the glandular epithelium atrophy, basically the same as the histopathology of 15% NaCl hot water solution gavage for 10 to 12 weeks Changes, the rat gastric mucosa atrophy became more obvious at 32 weeks. Scanning electron microscope showed that at 24 weeks, gastric mucosal cells were atrophied, glandular cavity enlarged and bleeding was observed; at 32 weeks, in addition to gastric mucosal cell atrophy and glandular cavity enlargement was more obvious, a large number of epithelial cell shedding and cell damage were also seen , Focal mucosal erosion. Transmission electron microscopy showed that at 24 weeks, the glands shrank, fibrous connective tissue proliferated around the glands, glandular cavity was irregular, gland cells atrophy, cell spacing increased, intracytoplasmic organelles decreased, secretory granules decreased and vacuolated, rough surface The endoplasmic reticulum was significantly expanded, and a small number of cells showed reduced nucleus euchromatin and increased heterochromatin. It was close to the nuclear membrane, and early apoptosis occurred. At 32 weeks, cell atrophy was more obvious, intracytoplasmic organelles decreased sharply, and early apoptosis The phenomenon of death is more common.

　　(3) Comparative Medicine Chronic Atrophic Gastritis (CAG) is a common disease of the digestive system. It has a high incidence, a long course, and a complex condition. It occupies an important position in precancerous lesions of the gastric mucosa. Although the etiology and pathogenesis of CAG have not yet been fully understood, the multiple occurrences and long-term chronic stimulation of acute gastritis are undoubtedly closely related to its occurrence and development. Experiments have confirmed that long-term stimulation of hot water can damage the gastric mucosa and cause inflammation; high salt can stimulate the gastric mucosa and cause parietal cells to fall off, thereby destroying the gastric mucosal barrier and causing atrophic gastritis; hot water and high salt are two factors Together, it aggravates the degree of gastric mucosal damage and accelerates the atrophy of the proper glands. The biggest feature of this model is that the selection of modeling factors is closer to human dietary habits. It has the advantages of short modeling cycle, simple method, high modeling rate, good reproducibility, etc., and it has shrinkage of mucosal glands and atrophy of glandular epithelium. There are pathological features such as lymphocytes and eosinophil infiltration in the lamina propria, but pathological phenomena such as intestinal metaplasia and pseudopyloric gland metaplasia are difficult to see. This model is more suitable for the study of the relationship between dietary habits and the occurrence, development and carcinogenesis of chronic atrophic gastritis.