[Animal Modeling] - Experimental Colitis Model in Young Rats

  1. Animal modeling materials: Healthy male SD rats, 5-6 weeks old; Drug: 2,4,6-trinitrobenzenesulfonic acid (TNB).

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

  3. Modeling principle: The TNB/ethanol modeling method belongs to the semi antigen induced model of the 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 disrupting the intestinal mucosal barrier, causing TNB to bind with intestinal tissue proteins to form a complete antigen, leading to delayed allergic reactions of the intestinal mucosal immune system to this antigen and causing damage to the intestinal mucosa.

  4. General changes after modeling: The model group showed loose hair and mental fatigue shortly after modeling, with mucopurulent and bloody stools starting at 6 hours, all at 24 hours, and relieved at 72 hours. After 1 week, mucopurulent and bloody stools disappeared, but loose stools still appeared, and symptoms completely disappeared after 3 weeks. The most severe symptom period in the model group was 24 hours after modeling. The control group did not experience mucus, pus, or bloody stools, and only showed loose hair within 72 hours, which then recovered. The weight loss in the model group was greater than that in the control group at 24 and 72 hours after modeling, and the weight gain at 3 and 4 weeks was lower than that in the control group.

  5. Pathological changes after modeling: The model group had the most severe mucosal damage 24 hours after modeling, with large ulcers forming but no transmural ulcers observed. Microscopically, epithelial cell detachment and necrosis, ulcer formation, destruction of crypt structures, infiltration of eosinophils and neutrophils were observed, but no obvious cryptitis or crypt abscess was observed. After one week, the ulcer basically healed, and the intestinal mucosa was mainly congested and edematous, with some intestinal walls thickening and infiltration of chronic inflammatory cells; The infiltration of lymphocytes and plasma cells was mainly observed at 2 and 3 weeks; At 4 weeks, the mucosal epithelial damage and inflammatory cell infiltration basically disappeared under the microscope. The control group only had mucosal congestion and edema 1 week ago, with loose submucosa under microscope, and no significant abnormalities remaining.