Fig. 6: rFGF1ΔHBS inhibits ADR-induced inflammation and oxidative stress in the kidney. | Cell Death & Disease

Fig. 6: rFGF1ΔHBS inhibits ADR-induced inflammation and oxidative stress in the kidney.

From: FGF1ΔHBS ameliorates chronic kidney disease via PI3K/AKT mediated suppression of oxidative stress and inflammation

Fig. 6

Analysis of renal tissues from mice with ADR-induced (10.5 mg/kg body weight) nephropathy treated for 5 weeks with rFGF1ΔHBS (0.5 mg/kg body weight) or buffer control; normal BALB/c mice served as additional controls. a Representative images and quantitation of immunofluorescence staining for F4/80. Scale bar, 50 μm. b Phosphorylation levels of ASK and JNK and expression levels of CD68, COL 4, and TGF-β1 as determined by western blot analysis (left panel) and quantitation using ImageJ software (right panel). c Real-time PCR analysis of Tnf-α, Il-1β, Tgf-β1, Fn1, and Acta2 mRNA expression. d Representative images and quantitation of DHE immunofluorescence. Scale bar, 50 μm. e ELISA analysis of MDA levels in each group. f Expression of Nrf2, NQO1, and SOD2 as determined by western blot analysis (left panel) and quantitation using ImageJ software (right panel). Data are presented as the mean ± SEM (n = 5–8). Panels a, d, e: *p < 0.05, ***p < 0.001; panels b, c, f: *p < 0.05, **p < 0.01, ***p < 0.001 versus Ctrl; #p < 0.05, ##p < 0.01, ###p < 0.001 versus ADR

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