动物造模,IgA肾病小鼠模型 z-bio 2021-12-16 246

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

　　Method: 12 BALB/c mice were randomly divided into normal group (6) and model group (6). The model group received a single intravenous injection of staphylococcal enterotoxin B (SEB) 0.8 mg/kg. Inject once a week for 3 consecutive weeks. After 4 weeks, the mice will have 24-hour urine protein quantification, urine microalbumin, renal function BUN, Scr, UA; protein index TP, ALB; liver function ALT, AST, ALP; blood lipids TC, TG, LDL, renal immunofluorescence IgA deposition, renal pathology HE, PAS, PASM, transmission electron microscope observation of Masson staining and superstructure of the kidney, as well as liver and small intestine HE staining, immunofluorescence IgA deposition changes.

　　Results: Compared with the normal group, the 24-hour urine protein quantification and urine microalbumin in the model group increased (P\u003c0.01), and the renal function indexes CREA and UA of the model group were higher than those of the normal group. Normal group (P\u003c0.05). ), BUN difference is not significant; model group mouse protein index TP, ALB difference is not significant; model group mouse liver function index AST level is higher than normal group (P\u003c0.05), ALT, ALP difference is not significant ; The blood lipid TG level of the model group of mice is lower than the normal group (P\u003c0.05), and the LDL level is higher than the normal group (P\u003c0.01). There is no significant difference in TC. Kidney immunofluorescence examination showed that there were a large amount of IgA deposits on the glomerular mesangium of the model group; the renal pathological damage of the mice in the model group was mild to moderate, and the immune complexes in the mesangial area of the model group increased; HE staining of the liver showed a small amount of IgA deposition. Inflammatory cell infiltration with partial hepatocyte necrosis, small intestinal villi defect, small intestinal villi are short and thin, the interval is obviously widened and part of the epithelium falls off, the central central tube in the middle of the kidney is obviously expanded, and the lymphocytes increase. Inflammatory cell infiltration is clearly visible.

　　Conclusion: Tail vein injection of mouse superantigen SEB can successfully replicate the animal model of IgA nephropathy.