动物造模,高尿酸血症 z-bio 2022-09-05 361

　　Objective To screen a stable rat model of hyperuricemia.

　　Methods The model was established with potassium oxonate, fructose and hypoxanthine alone or in combination, and the serum uric acid, creatinine, blood urea nitrogen, xanthine oxidase, aspartate aminotransferase, and serum uric acid levels in hyperuricemic rats prepared by different administration methods and time were observed. Alanine aminotransferase activity, liver and kidney pathological section changes, renal adenosine triphosphate-binding transporter G superfamily member 2 protein expression.

　　Results Compared with the normal group, the serum uric acid, blood urea nitrogen levels, AST and XO activities of the rats were significantly increased (P<0.05), the liver and kidney were slightly damaged, and the expression of ABCG2 protein in the kidneys was significantly increased after 7 days of modeling with potassium oxonate alone. Significantly decreased (P<0.05). Fructose and potassium oxonate combined with model establishment for 7 days significantly increased serum uric acid in rats (P<0. xo="" abcg2="" p="">0. 05); , blood urea nitrogen level and XO activity increased significantly (P<0. ast="" alt="" p="">0. 05), liver and kidney damage was not significant. After 7 days of hypoxanthine and potassium oxonate combined modeling, the levels of serum uric acid, creatinine, blood urea nitrogen, AST, ALT, and XO activities were significantly increased (P<0.05), and the liver and kidney were severely damaged. The expression level decreased (P<0.05).

　　Conclusion Potassium oxonate alone can establish a model of acute hyperuricemia with mild liver and kidney damage, fructose combined with potassium oxonate can establish a model of chronic hyperuricemia with minimal liver and kidney damage, and hypoxanthine combined with potassium oxonate can establish a model of chronic hyperuricemia with minimal liver and kidney damage. A model of acute hyperuricemia with severe liver and kidney damage was established.