IgA肾病小鼠模型 z-bo 2020-12-06 343

　　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) and model group (6). The model group received a single tail vein injection of staphylococcal enterotoxin B (SEB) 0.8 mg/kg, starting from the second week , Continuous injection for three weeks, after the end of the fourth week, the mice were tested for 24-hour urine protein quantification, urine microalbumin, renal function BUN, Scr, UA; protein indicators TP, ALB; liver function ALT, AST, ALP; blood lipid TC, TG, LDL, kidney immunofluorescence IgA deposition, renal pathology HE, PAS, PASM, Masson staining and transmission electron microscopy to observe the kidney ultrastructure, as well as the liver and small intestine HE staining, immunofluorescence IgA deposition changes. Results: Compared with the normal group, the 24-hour urine protein quantitative and urine microalbumin in the model group increased (P<0.01); the renal function indexes CREA and UA of the model group were higher than the normal group (P <0.05) There was no significant difference in BUN; there was no significant difference in protein index TP and ALB in the model group; the liver function index AST level 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; model group The blood lipid TG level of mice was lower than that of the normal group (P <0.05), and the LDL level was higher than that of the normal group (P <0.01). There was no significant difference in TC. Kidney immunofluorescence examination showed granular and massive IgA deposits in the glomerular mesangial area of the model group; mice in the model group had mild to moderate kidney pathological damage and increased immune complexes in the mesangial area; the liver of the model group HE staining shows a small amount of inflammatory cell infiltration accompanied by partial hepatocyte necrosis, small intestinal villi defect, intestinal villi become shorter and thinner, and the spacing is obviously widened, some of the epithelium falls off, the central central chylo duct is significantly dilated, and the lymphocytes increase, which is obvious Inflammatory cell infiltration.

　　 Conclusion: The tail vein injection of superantigen SEB in mice can successfully replicate the animal model of IgA nephropathy.