ObjectiveTo explore how dexamethasone (Dex) directly restores kidney podocyte function in adriamycin (ADR)-induced nephrotic model and the effects of Dex on the motility of podocytes,to analyze whether nephrin is a key signal molecule in the process. MethodsThe cultured podocytes were divided into three growps: ADR treated group,ADR+Dex group,blank control group. The analyses of podocytes function were performed using scrape-wound,Transwell migration assays and FITC-BSA. Quantitative real-time PCR and Western blot were used to test the expression of nephrin. Male SD rats were used to generate ADR-induced nephrology model,and randomly divided into three groups: ADR group,ADR+Dex group and normal group. At 7 d,14 d,21 d and 28 d after ADR injection,24 h urine protein was measured as well. Podocyte foot process effacement was observed under transmission electron microscopy. ResultsPodocytes’ motility,permeability of a monolayer of podocytes incubated with FITC-BSA,the expression of nephrin were higher in ADR group than those in blank control group (PPPPPP
