Fig. 2
SOCS1 therapies reduce oxidative stress in diabetic mouse aorta. a Representative images (scale bar, 40 μm; L Lumen) of O2•− production (DHE fluorescence; yellow dashed lines indicate atheroma), oxidative DNA damage (8-OHdG immunoperoxidase) and atherosclerotic lesion (Masson’s trichrome staining) in aortic 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). b, c Summary of quantitative evaluation of DHE- (b) and 8-OHdG- (c) positive cells per lesion area. d Quantitative analysis of atherosclerotic lesion size. Bars are the mean ± SEM of 6–8 (early model) and 7–10 (late model) mice per group. *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. e, f Pearson’s correlation analysis of DHE (e) and 8-OHdG (f) staining with atherosclerotic lesion size in mice at early and late intervention
