Fig. 4: rFGF1ΔHBS suppresses diabetes-induced renal inflammation and oxidative stress. | Cell Death & Disease

Fig. 4: rFGF1ΔHBS suppresses diabetes-induced renal inflammation and oxidative stress.

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

Fig. 4

Renal tissues were isolated from db/db mice treated for 12 weeks with rFGF1ΔHBS (0.5 mg/kg body weight) or buffer control; littermate db/m 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 renal tissues from each group. f Expression levels 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< 0.01, ***p< 0.001; panels b, c, f: *p < 0.05, **p< 0.01, ***p< 0.001 versus db/m; #p< 0.05, ##p< 0.01, ###p< 0.001 versus db/db

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