A new animal model of uric acid nephropathy
A new animal model of uric acid nephropathy
Current methods of preparing animal models of uric acid nephropathy are mainly through the concomitant administration of drugs that inhibit uric acid excretion and uric acid-producing raw materials such as xanthines, or through the administration of large quantities of adenine to produce secondary uric acid nephropathy. These two methods are not ideal for modeling. A new animal models of hy peruricemic nephropathy is described below.
Principle
Depending on the experimental method, the corresponding principles are different:
The basic principle of the novel animal model of uric acid nephropathy: In order to establish a new animal model of uric acid nephropathy, SD rats were fed with three different diets, namely, yeast, yeast plus adenine, and yeast plus adenine plus sardines, and the changes in serum uric acid (UA), creatinine (SCr), urea nitrogen (BUN) and renal tissues were observed. It was found that all three modeling methods could make serum uric acid, creatinine, and urea nitrogen significantly higher than those of the normal group, and the BUN and UASCr of the rats using the latter two modeling methods were significantly higher than those of the first one. The results indicated that the renal pathological changes in the animal model of yeast modeling were similar to those of human uric acid nephropathy. The yeast-induced disease model alone is a better animal model for primary uric acid nephropathy, while the latter two modeling methods are more consistent with the pathogenesis of secondary uric acid nephropathy in humans. Appliance The common application areas of the new animal model of uric acid nephropathy are as follows: The established rat model of hyperuricemia and uric acid nephropathy can be used to study the mechanism of the occurrence of nephropathy caused by high uric acid and to observe the preventive and therapeutic effects of drugs. Operation method A new animal model of uric acid nephropathy Principle According to the different experimental methods, the corresponding principles are also different: the basic principle of the new animal model of uric acid nephropathy: in order to establish a new animal model of uric acid nephropathy, SD rats were fed with three different formulations of diets, namely, yeast, yeast plus adenine and yeast plus adenine plus sardines, and the changes in serum uric acid (UA), creatinine (SCr) and urea nitrogen (BUN) and renal tissues were observed. It was found that all three modeling methods could make serum uric acid, creatinine, and urea nitrogen significantly higher than those of the normal group, and the BUN and UASCr of the rats using the latter two modeling methods were significantly higher than those of the first one. The results indicated that the renal pathological changes in the animal model of yeast modeling were similar to those of human uric acid nephropathy. The yeast-induced disease model alone is a better animal model for primary uric acid nephropathy, while the latter two modeling methods are more consistent with the pathogenesis of secondary uric acid nephropathy in humans. Materials and Instruments Subjects: Move The basic procedure of the new animal model of uric acid nephropathy can be divided into the following steps: Caveat 1. Changes in blood and urine indexes. After 21 days of modeling, the uric acid, blood creatinine and urea nitrogen of groups B, C and D were significantly higher than that of group A, indicating that the modeling of uric acid nephropathy was successful. The urea nitrogen values of groups B and C were significantly higher than those of group A. The pathological results of group B and C are shown in the following table. 2. Pathological findings: HE staining, 10×4× light microscopy, more lesions, most of the renal tubules and interstitium were involved; 10×10× light microscopy, focal interstitial fibrosis, accompanied by a large number of lymphocytes and monocytes infiltration, part of the renal unit atrophy, and some of the renal tubules showed cystic dilatation, epithelial atrophy; 10×20× light microscopy, interstitial cell atrophy, part of the glomerular volume is reduced, adhered to the wall of the capsule, and glomeruli are not connected with the wall of the capsule, and the glomeruli are not connected to the wall of the capsule. In 10×20× light microscopy, protein tubular pattern was seen in the distal renal tubules, and rectangular or amorphous urate crystals were seen in the tubular lumen of some renal tubules. For more product details, please visit Aladdin Scientific website.
① Rats.
Experimental reagents:
① Physiological saline.
Clean-grade male SD rats, weighing 150-180 g, were randomly divided into normal control group (group A, standard chow), group B (standard chow + 15 g, yeast), group C (standard chow + 10 g, yeast + 100 mg, adenine), group D (standard chow + 10 g, yeast + 80 mg, adenine + 5 g, sardine). sardines). Yeast, adenine and sardines were calculated per kg body weight per day. Based on the above grouping and formulation, the dosage of the formula was changed according to the weight change of rats (rats were weighed every 10 days). Yeast, adenine and sardines were mixed with a small amount of standard powder and then fed to the rats to ensure the consumption of the additives, and the feed shortage was supplemented. 21 days later, the animals were executed to remove the blood, and the left kidney of the rats was removed and fixed in formaldehyde solution.