Objective To establish a reasonable and stable rat model of uric acid nephropathy, and to provide a pathological model for screening and studying the treatment of uric acid nephropathy.
Methods The experimental rats were randomly divided into 3 model groups and normal groups. The model group was given 750 mg/kg potassium oxazinate combined with 150 mg/kg low-dose uric acid (M-A group), 750 mg/kg potassium oxazinate combined with 300 mg/kg medium dose uric acid (M-B group), 750 mg/kg potassium oxazinate combined with 600 mg/kg high-dose uric acid (M-C group), the normal group (Control group) was given 0.3% sodium carboxymethyl cellulose (100 g/mL), and the blood uric acid, blood creatinine, urea nitrogen, triglyceride Changes in cholesterol and other indicators, as well as pathological changes in the kidney.
Results Compared with the normal group, the serum uric acid in the three model groups was significantly higher than that in the normal group (P<0.01, P<0.05, P<0.05); The serum creatinine in M-B group and M-C group increased significantly (P<0.05, P<0.01); Triglycerides in M-B group were significantly lower than those in normal group (P<0.05); The renal pathological score of M-B group and M-C group was significantly higher than that of the normal group (P<0.01); Masson staining morphology showed that renal injury in the three model groups was more obvious than that in the normal group (P<0.05, P<0.01, P<0.01). The results of immunohistochemistry showed that the expression of CD68 in the three model groups increased compared with the normal group (P<0.05, P<0.01, P<0.01); Compared with the normal group, the expression of E-cadherin in M-B and M-C groups decreased significantly (P<0.01); α- Compared with the normal group, the expression of SMA in the three model groups increased (P<0.05, P<0.01, P<0.01).
Conclusion Potassium oxazinate (750mg/kg) combined with medium dose uric acid (300mg/kg) can be used as an ideal method to establish rat model of uric acid nephropathy.