动物造模,药效评价,非免疫性慢性肾衰竭 z-bio 2024-09-24 375

　　1. Modeling material animals: Male SD rats, 10-12 weeks old, weighing 180-220g; Medications: pentobarbital, benzalkonium bromide.

　　2. Modeling method: Anesthetize rats by intraperitoneal injection of pentobarbital (4mg/kg), fix the rats in a supine position on the operating table, remove the hair from the abdomen, disinfect the abdomen locally with benzalkonium bromide, and make a longitudinal incision along the midline of the abdomen to open the abdominal cavity. First, expose the left kidney and isolate the perirenal fat sac. Under a microscope, isolate the renal artery and its branches, revealing 3-4 branches of the renal artery. Ligature the 2 branches supplying the lower pole with a 3 × 0 line, and immediately turn pale about two-thirds of the lower left kidney. After observing for 3 minutes, reposition the left organ. Expose the right kidney, separate the right renal pedicle and right ureter under a microscope, ligate the entire renal pedicle and right ureter with 1 × 0 thread, and remove the right kidney. Observe the surgical field for no bleeding or exudation, and then suture layer by layer to close the abdominal cavity. The anesthesia and opening of the abdominal cavity in the sham surgery group are the same as above. After exposing the left and right kidneys, blunt separation of the renal capsule is sufficient.

　　3. The modeling principle is to establish a rat model of non immune chronic renal failure by ligating the left extrarenal artery branch and removing the right kidney.

　　4. After the 12th week of the modeling experiment, the levels of blood creatinine and urea nitrogen in the modeling group were significantly higher than those in the sham surgery group; The arterial systolic pressure and 24-hour urinary protein content in the model rats were significantly higher than those in the sham surgery group. Under light microscopy, most of the glomeruli in the model group showed severe or even complete sclerosis, with significant thickening of the walls of small arterioles entering and exiting the glomeruli, tubular atrophy, and increased infiltration and fibrosis of inflammatory cells in the interstitium. The glomerular sclerosis score in the model group was significantly higher than that in the sham surgery group.