动物造模,药效评价,结肠炎 z-bio 2024-07-17 322

　　1. Modeling material animals: Healthy male SD rats, 5-6 weeks old; Drug: 2,4,6-trinitrobenzenesulfonic acid (TNB).

　　2. Modeling method: After fasting for 48 hours, under pentobarbital anesthesia, a 2mm diameter silicone tube was inserted from the anus into the intestine about 8cm deep. The model group was injected with 0.25ml TNB150mg/kg dissolved in 50% ethanol, while the control group was injected with 0.7ml NS for one-time enema.

　　3. Modeling principle TNB/ethanol modeling method belongs to the semi antigen induced model under normal immune system. When TNB/ethanol enema is performed, ethanol acts as an organic solvent to dissolve the mucus on the surface of the intestinal mucosa, temporarily destroying the intestinal mucosal barrier, allowing TNB to bind with intestinal tissue proteins to form a complete antigen, leading to delayed hypersensitivity reactions of the intestinal mucosal immune system against the antigen and causing damage to the intestinal mucosa.

　　4. General changes after modeling: The model group showed loose hair and lethargy shortly after modeling. Mucous purulent stools began to appear at 6 hours, and all mucous purulent stools appeared at 24 hours. After 72 hours, the symptoms improved. Mucous purulent stools disappeared after 1 week, but loose stools still appeared. Symptoms completely disappeared after 3 weeks. The most severe symptoms in the model group occurred 24 hours after modeling. The control group did not experience mucous purulent stools, only loose hair appeared within 72 hours, and then recovered. The weight loss of the model group was greater than that of the control group at 24 and 72 hours after modeling, and the weight gain was lower than that of the control group at 3 and 4 weeks.

　　5. Pathological changes after modeling: The model group showed the most severe mucosal damage 24 hours after modeling, with the formation of large ulcers but no transmural ulcers. Under the microscope, epithelial cell shedding and necrosis, ulcer formation, crypt structure destruction, eosinophil and neutrophil infiltration were observed, but no obvious crypt inflammation or crypt abscess was found. The ulcer has basically healed within one week, and the intestinal mucosa is mainly congested and edematous, with some thickening of the intestinal wall and infiltration of chronic inflammatory cells; At 2 and 3 weeks, lymphocyte and plasma cell infiltration were predominant; At 4 weeks, the mucosal epithelial damage and inflammatory cell infiltration under the microscope basically disappeared. The control group only had mucosal congestion and edema one week ago, and the submucosal layer was loose under the microscope, with no significant abnormalities observed in the rest.