动物造模,高尿酸血症动物模型 z-bo 2021-01-07 305

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

　　 Method: After 30 days of high-fat feeding of quail, adenine (50 mg/head) is forcibly fed for 7 days to establish a quail hyperuricemia model. After 22 days of observation, blood will be collected to detect uric acid, xanthine oxidase and creatinine in the blood. (CRE), urea nitrogen (BUN), triglycerides (TG), low-density lipoprotein (LDL), high-density lipoprotein (HDL), total cholesterol (CHO), xanthine oxidase (XOD), liver fat Enzyme (HL), lipid protein lipase (LPL), adenosine dehydrogenase (ADA) lipid metabolism index for histopathological examination of joints and kidneys.

　　Result: The blood uric acid of the model control group increased significantly (P \u003cu003c0.01), and CRE, BUN, TG, LDL, XOD increased significantly (P \u003cu003c0.05 or P \u003cu003c0\→). .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 swelled. X-ray examination showed that the bone density of the toes was reduced, and part of the joint surface was damaged due to osteolytic injury. Pathological examination revealed joint synovial hyperplasia, infiltration of a large number of inflammatory cells, some of which were replaced by fibrous connective tissue, and uric acid crystals in the interstitium of renal tubules and renal tissue. The tubules of the spleen are slightly dilated, accompanied by renal interstitial fibrosis. Many inflammatory cells infiltrate.

　　 Conclusion: This model has kidney damage, 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.