高尿酸血症模型 z-bo 2020-12-30 318

　　Purpose: To establish models of hyperuricemia in acute mice and chronic rats, and use positive drugs to verify the curability of the two models, and to provide model tools for the development of anti-hyperuric acid drugs.

　　Methods: Acute gout model mice were modeled by intraperitoneal injection of hypoxanthine combined with subcutaneous injection of potassium oxazine. The positive group was given allopurinol tablets half an hour after the model was modeled. Blood uric acid, blood creatinine, and serum were measured 2 hours after model creation. Urea nitrogen and liver xanthine oxidase (XOD) activity. Chronic gout rats were given adenine and ethambutol hydrochloride daily to create a model. The positive group was given allopurinol tablets every day. After 21 consecutive days, blood uric acid, blood creatinine, serum urea nitrogen, liver XOD activity and renal tissue disease were detected. Physical testing.

　　Results: The blood uric acid and blood creatinine of acute and chronic gout model animals were significantly increased (P<0.05). In chronic gout rats, serum urea nitrogen and liver XOD activity were also significantly increased (P<0.05), and renal tubular interstitial damage And urate crystals aggravated, and the score increased significantly (P<0.05). The positive drug allopurinol can significantly reduce the blood uric acid value of acute and chronic hyperuric acid animals, reduce the blood creatinine value and liver XOD activity of chronic hyperuric acid animals, improve kidney damage and reduce urate crystals (P<0.05).

　　Conclusion: The method used in this experiment is suitable for establishing acute and chronic hyperuricemia animal models, and can be used for drug pharmacodynamic observation.