[Dexamethasone Blocks Adriamycin-induced Podocytes'Mobility via Impacting Nephrin Expression]

To 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.

The 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.

Podocytes' 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 (P<0.05); on the contrary, the indexes above in Dex+ADR group were decreased when compared with ADR group (P<0.05). 24 h urine protein increased significantly at day 14 (vs. normal group P<0.001) and peaked at day 28 in ADR rats (vs. normal group P<0.001), whereas decreased at day 14, 21 and 28 in Dex+ADR group (vs. ADR group, P<0.001). The FWP of ADR-treated rats was greater than normal group and Dex+ADR group (P<0.01).

Dex impacts the expression of nephrin, relieves the enhanced motility induced by ADR and decreases urine protein level.