Objective To establish a reasonable and stable rat model of uric acid nephropathy, and to provide a pathological model for screening and research on the treatment of uric acid nephropathy.
Methods Experimental rats were randomly divided into 3 modeling groups and normal group. The modeling group was given 750 mg/kg potassium oxonate combined with 150 mg/kg low-dose uric acid (group M-A), 750 mg/kg potassium oxonate combined with 300 mg/kg medium-dose uric acid (group M-B), and 750 mg/kg oxonate Potassium 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 serum uric acid, serum creatinine, blood urea nitrogen, Changes in triglyceride, cholesterol and other indicators as well as pathological changes in the kidneys.
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 the M-B group and the M-C group was significantly increased (P<0.05, P<0.05). 0.01); triglyceride in M-B group was significantly lower than that in normal group (P<0.05); renal pathological score in M-B group and M-C group was significantly higher than that in normal group (P<0.01); Masson staining morphological showed that 3 Compared with the normal group, the kidney injury in each model group was more obvious (P<0.05, P<0.01, P<0.01). The results of immunohistochemical inflammatory CD68 showed that compared with the normal group, the expression levels of the three model groups increased (P<0.05, P<0.01, P<0.01); compared with the normal group, the expression levels of E-Cadherin in the M-B and M-C groups Compared with the normal group, the expression of α-SMA was increased in the three model groups (P<0.05, P<0.01, P<0.01).
Conclusions Potassium oxonate (750mg/kg) combined with medium-dose uric acid (300mg/kg) can be used as an ideal method to construct a rat model of uric acid nephropathy.