动物造模,IgA肾病小鼠模型 z-bio 2022-11-04 202

　　Objective: To establish a mouse model of IgA nephropathy and observe the biochemical and pathological characteristics of the model.

　　Methods: Twelve BALB/c mice were randomly divided into normal group (6 mice) and model group (6 mice). The model group received a single tail intravenous injection of staphylococcal enterotoxin B (SEB) of 0.8 mg/kg. From the second week, the mice were injected for three consecutive weeks. At the end of the fourth week, the 24 hour urine protein quantity, urine microalbumin, and renal function BUN, Scr, UA of the mice were measured; Protein indicators TP and ALB; Liver function ALT, AST, ALP; TC, TG, LDL of blood lipids, deposition of immunofluorescent IgA in kidney, HE, PAS, PASM, Masson staining and transmission electron microscopy of kidney pathology, HE staining of liver and small intestine, deposition of immunofluorescent IgA.

　　Results: Compared with the normal group, the 24 h urine protein quantity and urine microalbumin in the model group increased (P<0.01); The renal function indexes CREA and UA in the model group were higher than those in the normal group (P<0.05), and there was no significant difference in BUN; There was no significant difference in protein indexes TP and ALB in model group; The AST level of liver function index in the model group was higher than that in the normal group (P<0.05), and there was no significant difference in ALT and ALP; The TG level of blood lipid in the model group was lower than that in the normal group (P<0.05), and the LDL level was higher than that in the normal group (P<0.01), with no significant difference in TC. The renal immunofluorescence test showed that the glomerular mesangial area of the model group mice showed granular and agglomerated IgA deposits; In the model group, the pathological changes of the kidney were mild to moderate, and the immune complexes in the mesangial region increased; In the model group, HE staining of mice liver showed that a small amount of inflammatory cell infiltration accompanied by partial necrosis of hepatocytes, intestinal villi defect, intestinal villi becoming shorter and thinner, the spacing being significantly widened, part of the epithelium falling off, central chylous duct expanding significantly, lymphocytes increasing, and obvious inflammatory cell infiltration.

　　Conclusion: The mouse model of IgA nephropathy can be successfully reproduced by tail vein injection of superantigen SEB.