| Objective: To explore the expression and and the potential role of SGK3 and Ezrin in the mouse model of FSGS.Methods: 1. 18 BALB/C male mice(8 week old) were divided into control group and model group. Focal segemental glomerular sclerosis(FSGS) mouse model was induced by a single tail vein injection of adriamycin(ADR,10.5mg/Kg weight). The control group was administrated an equivalent intravenous volume of normal saline vehicle. 2. Mice spot urine was collected at day 0, 14 and 28 after ADR injection, and the urinary protein and creatinine excretion rate were measured. Blood samples were collected at day 28, and the plasma levels of urea, albumin and creatinine were detected. 3. The pathological changes of renal tissue were detected by periodic acid-Schiff(PAS) staining. 4. The expression level of SGK3 and Ezrin were evaluated by immunohistochemistry and Western bloting analyses.Results: 1?Construction of FSGS mouse model: The urinary protein creatinine ratio(UTP/Ucr) was higher in the model group than in the control group at day 14(p<0.05),and reached the peak at day 28(p<0.01). But the plasma levels of urea, albumin and creatinine of the model group did not change significantly. PAS staining showed that mice with ADR-induced nephropathy exhibited mesangial expansion, well developed exudative(fibrin-cap) lesions, glomerular sclerosis, tubular collapse, cast formation at day 28. 2?Immunohistochemistry: Compared with the control group, the expression level of SGK3 and Ezrin in model group decreased significantly(P<0.01). 3?Western blotting:The expression levels of SGK3 and Ezrin in the model group decreased significantly as compared with those in the control group(P<0.05).Conclusions: Both SGK3 and Ezrin were involved in the pathogenesis of adriamycin induced FSGS in mice. |
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