动物造模,肾病小鼠模型 z-bio 2022-09-24 260

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

　　Methods: Twelve BALB/c mice were randomly divided into a normal group (6 mice) and a model group (6 mice). The model group was given 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 fourth week, the 24-hour urine protein quantification, urine microalbumin, renal function BUN, Scr, UA; protein indexes TP, ALB; liver function ALT, AST, ALP; blood lipids TC, UA The conditions of TG and LDL, the deposition of immunofluorescence IgA in the kidneys, the ultrastructure of the kidneys observed by HE, PAS, PASM, Masson staining and transmission electron microscopy, as well as the deposition changes of the liver and small intestine by HE staining and immunofluorescence IgA.

　　Results: Compared with the normal group, the 24-hour urine protein quantification and urinary microalbumin of the model group were increased (P < 0.01); the renal function indexes CREA and UA of the model group were higher than those of the normal group (P < 0.05). , BUN had no significant difference; the model group had no significant difference in protein indexes TP and ALB; the model group had higher liver function indexes AST than the normal group (P < 0.05), and there was no significant difference in ALT and ALP; the model group had no significant difference in ALT and ALP; The blood lipid TG level of mice was lower than that of the normal group (P < 0.05), the LDL level was higher than that of the normal group (P < 0.01), and there was no significant difference in TC. The kidney immunofluorescence examination showed that the IgA deposits in the mesangium of the model group were granular and clump-like; the kidneys of the model group were slightly to moderately damaged, and the immune complexes in the mesangium increased; the liver of the model group mice HE staining showed a small amount of inflammatory cell infiltration accompanied by partial hepatocyte necrosis, small intestinal villi defects, shortening and thinning of intestinal villi, significantly widened spacing, partial epithelium shedding, significant expansion of the central chyle duct, and increased lymphocytes, which were clearly visible. Inflammatory cell infiltration.

　　Conclusion: The animal model of IgA nephropathy can be successfully replicated by tail vein injection of superantigen SEB in mice.