RESUMO
Objective To establish a mouse model of IgA nephropathy and to observe its biochemical and pathological characteristics. Methods Twelve BALB/c mice were randomly divided into the normal group and model group, with 6 mice in each group. Mice in the model group received an intravenous injection of 0. 8 mg/kg superantigen staphylococcal enterotoxin B (SEB) into the tail vein once a week for three weeks. At the end of the 4th week, the mice were sacrificed, and the 24 h-urinary protein, urinary microalbumin, the renal function indicators BUN, Scr and UA were measured, levels of liver function indicators ALT, AST, ALP, and the blood lipid levels of TC, TG, and LDL were determined, the renal morphological changes were examined by pathology using HE, PAS, PASM and Masson staining, and by electron microscopy, the IgA deposition in the renal tissue was observed with immunofluorescence, and the liver and small intestine were observed by pathology using HE staining. Results Compared with the normal group, the mice of model group showed increased 24-hour urinary protein and urinary microalbumin (P<0. 01), increased CREA and UA (P<0. 05), but not significantly changed BUN, TP and ALB. The liver function indicator AST was significantly increased (P<0. 05), but ALT and ALP were not significantly changed. The blood lipid TG was significantly decreased (P<0. 05) and LDL increased (P<0. 01), while the TC was not significantly changed. The kidney tissues had moderate histological changes, and immunofluorescence observation showed granular or massive IgA deposition in the renal glomerular mesangium. The liver tissue had some inflammatory cell infiltration and hepatocyte necrosis. The small intestine showed slender and shortened villi with widened inter-villous space and sloughed off epithelial cells, dilated central lacteal, and lymphocyte infiltration. Conclusions A mouse model of IgA nephropathy can be successfully established by tail vein injection of superantigen staphylococcal entrotoxin B.
RESUMO
Pyroptosis is activated caspase-1 trigger special programmed cell. Recent studies have confirmed the py-roptosis in renal cells plays an important role. GSDMD cleavage caspase-1 regulating the downstream inflammatory cytokines maturation、release and triggering inflammation and pyroptosis. From renal inflammatory injury caused by NLRP3 activation, pyroptosis from GSDMD breakage, the review try to explain the NLRP3-caspase-1-GSDMD drived pyroptosis in renal inflammation injury to explore the essence of kidney inflammatory damage.
RESUMO
Pyroptosis is activated caspase-1 trigger special programmed cell. Recent studies have confirmed the py-roptosis in renal cells plays an important role. GSDMD cleavage caspase-1 regulating the downstream inflammatory cytokines maturation、release and triggering inflammation and pyroptosis. From renal inflammatory injury caused by NLRP3 activation, pyroptosis from GSDMD breakage, the review try to explain the NLRP3-caspase-1-GSDMD drived pyroptosis in renal inflammation injury to explore the essence of kidney inflammatory damage.