[Animal Modeling]-Quail hyperuricemia animal model

  Objective: To study the animal model of quail hyperuricemia and lipid metabolism.

  Method: After giving quail high fat for 30 days, take adenine (50 mg/head) orally for 7 days to establish a quail hyperuricemia model. Creatinine (CRE), Urea Nitrogen (BUN), Triglycerides (TG), Low Density Lipoprotein (LDL), High Density Lipoprotein (HDL), Total Cholesterol (CHO), Xanthine Oxidase (XOD), Liver Lipase (HL), lipoprotein lipase (LPL), adenosine dehydrogenase (ADA) lipid metabolism indicators require histopathological examination of joints and kidneys.

  Results: The blood uric acid of the model control group animals increased significantly (P\u003c0.01), CRE, BUN, TG, LDL and XOD increased significantly (P\u003c0.05 or P\u003c0) ..01), serum CHO , LPL, ADA, HDL content was significantly reduced (P\u003c0.05). After modeling, the animal’s toe joints were significantly swollen, and the surrounding soft tissues were swollen. X-rays showed that the bone density of the toes was reduced, and part of the joint surface was damaged due to osteolytic injury. Pathological examination showed joint synovial hyperplasia, accompanied by a large number of inflammatory cell infiltration, some of which were replaced by fibrous connective tissue, uric acid crystals between the renal tubules and renal tissue, part of the renal tubules dilated, infiltrating renal interstitial fibrosis, and Accompanied by many inflammatory cells.

  Conclusion: This model suffers from kidney diseases, such as joint swelling and kidney uric acid deposition, and is related to impaired lipid metabolism. The pathological mechanism is related to the activity of XOD and ADA-related lipid metabolism enzymes.