Fig. 3

Evolution of vascular complications: oxidative stress and vascular reactivity of mesenteric artery. a Higher panel. Visualization of dihydroethidine (DHE) representative immunofluorescent staining of ROS in rats’ liver (a) and mesenteric artery (b) during the study, at the beginning (M0) and after 2 (2M) and 8 (8M) months of normal diet (ND), normal diet + fructose (HF), high fat diet (HFD) and HFD + fructose (HFHF). Bottom panel. Corresponding cumulative data. Results are shown as mean ± SEM of 5 different experiments. * Significant results versus age-matched ND-rats and # between HFD- and HFHF-rats. Bar scale = 100 μm. b Concentration–relaxation curves to acetylcholine (ACh) in mesenteric artery rings with endothelium from control-rats (M0), normal diet-rats (ND, ) after 8 months of diet and normal diet + fructose (HF, ●), high fat diet (HFD, □) and HFD + fructose (HFHF, ■). Experiments were performed in the presence of indomethacin (10⁻⁵ M) and N^ω-nitro-l-arginine (L-NA, 10⁻⁴ M) to rule out the formation of vasoactive prostanoids and NO, respectively (EDHF-mediated component). Results are shown as means ± SEM of 5 different rats. *P < 0.05 represents a significant effect