Fig. 8: AKT mediates the protective effects of FGF1^ΔHBS on podocytes challenged with ADR.

a–c Analysis of mouse podocytes pretreated with rFGF1^ΔHBS (10 or 100 ng/mL for 1 h) and exposed to ADR (0.5 μg/mL for 12 h). a Phosphorylation levels of AKT and GSK-3β and protein expression levels of Nrf2, NQO1, and SOD2 as determined by western blot analysis. b Representative images and quantitation of DHE immunofluorescence. Scale bar, 50 μm. c Real-time PCR analysis of Tnf-α, IL-1β, TGF-β1, Fn1, and Acta2 mRNA expression. d, e. Cells were transfected with control or AKT siRNA, pretreated with FGF1^ΔHBS (100 ng/mL) for 1 h and incubated with adriamycin (0.5 μg/mL) for an additional 12 h. d Phosphorylation levels of AKT and GSK-3β and protein expression levels of GSK-3β, Nrf2, NQO1, and SOD2 as determined by western blot analysis (left panel) and quantitation using ImageJ software (right panel). e Real-time PCR analysis of TGF-β1, Tnf-α, and IL-6 mRNA levels. f Schematic diagram of the FGF1^ΔHBS-mediated inhibition of inflammation and oxidative stress in mouse podocytes challenged with HG or ADR. Data from three independent measurements are presented as the mean ± SEM. Panel b: ***p < 0.001; panel c: *p < 0.05, **p < 0.01 versus Ctrl; ^#p < 0.05, ^##p < 0.01 versus ADR; panel D: *p < 0.05, **p < 0.01, ***p < 0.001; panel e: **p < 0.01, ***p < 0.001 versus ctrl siRNA; ^###p < 0.001 versus ctrl siRNA + ADR; ^$p < 0.05 versus ctrl siRNA + ADR; ^&&p < 0.01; ^&&&p < 0.001 versus ctrl siRNA + ADR + FGF1^ΔHBS