动物模型,慢性萎缩性胃炎 z-bo 2020-08-07 543

　　(1) Replication method Adult rats are injected subcutaneously with 0.3ml/mouse of the same strain of rat gastric mucosa with normal saline tissue homogenate and adjuvant 1:1, and the injection is repeated once at 3 to 4 weeks. While performing the above-mentioned active immune stimulation, fasting for a single day and free eating for both days for 6 consecutive weeks. Or use the drained bile from patients without purulent inflammation, give 12.5ml/kg body weight to the rat by gavage (fast 4h before gavage without water), 5h later, give 12.5ml/kg body weight of 50℃ hot water in the same way, once /d, for 10 consecutive weeks. During the entire modeling period, the animals' mental state, activity, coat gloss and appetite were continuously observed, and their body weight was measured once a week. After modeling, the gastric mucosal pH, blood flow, and potential difference of the model animals were measured. The appearance of the gastric lesions was observed with naked eyes. The gastric mucosal thickness, inflammatory cell infiltration status and intestinal metaplasia were examined under light microscope.

　　(2) Model characteristics: Active immunity plus hunger and satiety stimulation for 7 weeks, model animals are atrophy, less active, inactive, tired, sparse and dull coat, weight loss gradually, gastric mucosa surface is rough and dry, less mucus, color Gray, punctate or flaky bleeding, irregular gastric mucosal folds, defects, superficial mucus cell interstitial expansion, edema, lamina propria hyperplasia, submucosal infiltration of eosinophils and lymphocytes, focal pyloric gland area Intestinal metaplasia. Active immunization plus bile and hot water gavage stimulation for 10 weeks, the pH value of the gastric mucosa of the model animals was significantly increased, the blood flow and the potential difference were significantly decreased, the gastric mucosa was thinned, the glands were reduced, inflammatory cell infiltration and intestinal metaplasia. After stopping stimulation for 5 weeks, the symptoms and histomorphological changes can still maintain the above pathological characteristics.

　　(3) Comparative medicine. The influence of immune factors on the etiology of chronic atrophic gastritis has received widespread attention. Based on the serum immunological examination and the distribution of gastric lesions, Strickland et al. divided atrophic gastritis into two independent types, type A and type B. Type A gastritis was positive for serum parietal cell antibodies, also known as autoimmune gastritis. The pathogenic factors of this model are autoimmune factors, which make the animal produce antibodies against gastric parietal cell mitochondria and factor antibodies, thereby activating lymphokines and complement, coupled with irregular diet, hunger and fullness, or imitating bile reflux and hot water stimulation, Eventually lead to gastric lesions, manifested by increased gastric mucosal pH, decreased glands, mucosal thinning, decreased blood flow and potential difference, inflammatory cell infiltration, intestinal metaplasia, similar to the pathological characteristics of human chronic atrophic gastritis. At 5 weeks after the model was formed, the above-mentioned pathological characteristics were maintained, showing that the method of this model is simple, the index is clear, and the characteristics are stable. It is suitable for the study of the immunological mechanism of chronic atrophic gastritis and the observation of the therapeutic effect of drugs.