IgA肾病小鼠模型,动物造模 z-bo 2021-10-29 628

　　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 tail vein injection of staphylococcal enterotoxin B (SEB) 0.8 mg/kg. At the beginning of each week, injections for 3 consecutive weeks, after the end of the 4th week, the mice 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, kidney immunofluorescence IgA deposition, renal pathology HE, PAS, PASM, Masson staining and transmission electron microscopy to observe the upper structure of the kidney and the liver and small intestine HE staining, immunofluorescence IgA deposition changes.

　　Result: 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. (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 was lower than the normal group (P(u003c0.05), and the LDL level was higher than the normal group (P\u0.01c0.01). There was no significant difference in TC. The immunofluorescence test of the kidney showed that The glomerular mesangium of the model group has granular and large amounts of IgA deposits; the mice in the model group have mild to moderate renal pathological damage and the immune complexes in the mesangial area. They show an increase in body; the model group HE staining of the liver showed part of hepatocyte necrosis, small intestinal villi defect, small intestinal villi are short and thin, and the interval is obviously widened, some epithelium has fallen off and a small amount of inflammatory cell infiltration in the center has been shown. Among them, the central canal of Cairo is obviously expanded and lymphocytes are increased. Inflammation Cell infiltration.

　　 Conclusion: Using the superantigen SEB to inject mice into the tail vein, the animal model of IgA nephropathy can be successfully replicated.