Fig. 6: Anti-VEGFR2 F(ab′)2-SS31 reduced oxidative stress, inflammation, and fibrosis in DN mice.

a Immunohistochemical staining (brown) of nitrotyrosine, a marker of peroxidation. Scale bar, 100 μm. b Quantitative analysis of nitrotyrosine staining in a. c, d SOD and MDA level changes in DN mice after different treatments. e Representative photomicrographs of F4/80 staining, a marker of macrophage. Scale bar, 50 μm. f Quantitative analysis of F4/80 staining. g, h Renal cytokine TNF-α and IL-6 alternation in DN mice after different treatments. i Representative photomicrographs of α-SMA, a marker of fibroblast. Scale bar, 50 μm. j Quantitative analysis of α-SMA expression. All data are expressed as the mean ± s.d. Statistical significance was calculated using a one-way ANOVA and post-hoc test. n = 6 mice in each group, n.s. no significant difference, *p < 0.05, **p < 0.01, ***p < 0.001 as compared with DN group; n.s. no significant difference, #p < 0.05, ##p < 0.01, ###p < 0.001 between groups as indicated. DN diabetic nephropathy, VEGFR2 vascular endothelial growth factor receptor 2, SOD superoxide dismutase, MDA malondialdehyde, TNF-α tumor necrosis factor-α, IL-6 interleukin-6, α-SMA α-smooth muscle actin. Source data are provided as a Source Data file.