Abstract: Objective To investigate the effects of prednisone on the expressions of FAK and Pyk2 in the kidneys of rats with
adriamycin-induced nephritis. Methods Thirty SD rats were randomized into normal control group, adriamycin-induced
nephritic model group, and prednisone treatment group (n=10). Prednisone was administered at 10 mg/kg once daily in
nephritic rats starting since the 7th day after adriamycin injection. Twenty-four-hour proteinuria was measured in the rats at
different time points, and renal tissue histology was examined using transmission electron microscope. The expression levels
of Pyk2, FAK and nephrin mRNA in the renal tissue were detected tested by RT-PCR, and the protein expressions of FAK,
Pyk2, phosphorylated Pyk2 and phosphorylated FAK-Tyr397 were detected by Western blotting; immunohistochemistry was
used for detecting nephrin protein expression in the kidney. Results Compared with the normal control group, the rats with
adriamycin-induced nephritis showed significantly increased proteinuria (P<0.01), which was obviously lowered by
prednisone treatment (P<0.01). Transmission electron microscopy revealed extensive fusion of the foot processes of the
podocytes in the model group. Prednisone treatment promoted nephrin expression in the kidney (P<0.05). Compared with the
control group, the model and prednisone treated groups showed significantly lowered nephrin mRNA expression (P<0.01) but
increased FAK mRNA expression (P<0.01), but prednisone-treated group had a higher nephrin mRNA expression than the
model group (P<0.05). The model group exhibited significantly increased expressions of FAK total and phosphorylated
proteins, P-FAK/FAK, and P-Pyk2/Pyk2 (P<0.01), which were all lowered in the treatment group (P<0.01). Correlation analysis
suggested that the expressions of FAK mRNA, FAK, pFAK, Pyk2 mRNA and pPyk2/Pyk2 were positively correlated with
proteinuria (r=0.819, 0.750, 0.838, 0.762, 0.934, respectively, P<0.01). Conclusions Adriamycin increases phosphorylated FAK
and Pyk2 expressions to mediate kidney injury in rats. Prednisone inhibits Pyk2 and FAK activation, decreases proteinuria,
and alleviates podocyte lesions to protect the glomerular filtration barrier.