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. 2017 Oct 30;7:14357. doi: 10.1038/s41598-017-14733-x

Figure 4.

Figure 4

Effects of sulforaphane and pyridoxamine treatment on systemic and vascular oxidative stress in GK rats compared with nondiabetic Wistar (W) rats. Representative DHE-stained aorta artery sections reflect O2· production with the different treatments (AE). The endothelium is facing up in all layers. At identical settings, fluorescence in diabetic GK (B) was markedly increased compared with normal vessel (Wistar, A). Note the increased fluorescence reflecting O2· levels in the endothelium, intima, and media of GK aorta. DHE fluorescence decreased in the diabetic GK rats treated with SFN (GKS, C), PM (GKP, D) and SFN + PM (GKSP, E). Panel (K) contains quantification of the fluorescence ethidium signal in the different groups of arteries. Representative mesenteric sections showing nitrotyrosine staining in nondiabetic Wistar (F), diabetic GK (G), and diabetic GK rats treated with SFN (GKS, H), PM (GKP, I) and SFN + PM (GKSP, J). Panel (L) contains quantification of the green fluorescence in the different groups of arteries. (M) Urinary 8-hydroxydeoxyguanosine (8-OHdG) levels in the different groups of rats. Data are expressed as mean ± SE (n = 12). *P < 0.05, ***P < 0.001 vs Wistar group; ϕP < 0.05, ϕϕP < 0.01, ϕϕϕP < 0.001 vs GK group.