Fig. 1

SOCS1-targeted therapies attenuate oxidative stress damage in diabetic kidneys. a Representative micrographs (scale bar, 20 μm) of O₂•⁻ production (DHE fluorescence), oxidative DNA damage (8-OHdG immunoperoxidase), and renal morphology (Masson’s trichrome staining) in paraffin-embedded kidney sections from diabetic apoE-deficient mice after early intervention with SOCS1-recombinant adenovirus (Control, Ad-null, and Ad-S1 groups) and SOCS1 peptidomimetic (Veh and miS1 groups) and late intervention with peptidomimetic (Veh, Mut, and miS1 groups). White dashed lines and asterisks denote DHE staining in glomeruli and tubules, respectively. b, c Quantification of DHE- (b) and 8-OHdG- (c) positive cells and in renal compartments. d Measurement of 8-OHdG levels in serum and urine samples. e Quantitative assessment of renal fibrosis in Masson-stained sections from diabetic mice at early and late diabetes. f Serum creatinine and albuminuria (UACR) levels in the experimental model. g Real-time PCR analysis of tubular injury marker Kim1 in diabetic kidneys; values were calculated after normalization to 18S and expressed as relative mRNA level compared with non-diabetic mice. Horizontal dotted lines represent the mean values for non-diabetic mice. Bars represent the mean ± SEM of 6–8 (early model) and 7–10 (late model) mice per group. Groups were analyzed separately using ANOVA with Bonferroni post-hoc test. ^*P < 0.05 vs Control, ^#P < 0.05 vs Ad-null, ^$P < 0.05 vs respective Veh (early or late model), and ^&P < 0.05 vs Mut