Table 1.
Mean body weight gained, blood glucose and glycated haemoglobin levels at the end of the experiment of normal and diabetic rats with or without 3′, 4′-dihydroxyflavonol (DiOHF, 1 mg/kg s.c. daily for 7 days) treatment.
Figure 1.
ROS measurement in intact mesenteric arteries.
A, Superoxide, B, DCFDA-induced flurorescence levels and C, NADPH-oxidase activity was increased in diabetic arteries which was reduced with DiOHF treatment. A, Superoxide levels in diabetic arteries were attenuated by the presence of L-NNA (100 µM), indicating eNOS uncoupling. n = 9–10 experiments. * p<0.05, ** p<0.01, *** p<0.001.
Figure 2.
Vascular function in mesenteric arteries.
Cumulative concentration-response curves to A, ACh, B, SNP, C, ET1 and D, basal NO release in endothelium-intact mesenteric arteries. In each group of experiments (A, B), mesenteric arteries were precontracted with phenylephrine to similar level: (A) normal 59±3, normal+DiOHF 59±3, diabetic 62±2, diabeticDiOHF 60±3, (B) normal 58±2, normal+DiOHF 57±3, diabetic 61±3, diabeticDiOHF 59±4%KPSS, n = 5–12 experiments. Results are shown as mean±SEM. * p<0.05, ** p<0.01. See Table 2 or results section for pEC50 and Rmax values.
Table 2.
Effect of L-NNA, ODQ and potassium channel blockers on ACh-induced relaxation of mesenteric arteries from normal and diabetic rats with or without 3′, 4′-dihydroxyflavonol (DiOHF, 1 mg/kg s.c. daily for 7 days) treatment in the presence of indomethacin.
Figure 3.
Contribution of NO to endothelium-dependent relaxation in mesenteric arteries.
NO-mediated relaxation in mesenteric arteries isolated from A, normal, B, diabetic, C, normal+DiOHF, D, diabetic+DiOHF rats. In each group of experiments, arteries were precontracted to similar level: A, 57±3, B, 58±2, C, 61±4, D, 59±2%KPSS, n = 9–15 experiments. Results are shown as mean±SEM. See Table 2 for values.
Figure 4.
Contribution of EDHF to endothelium-dependent relaxation in mesenteric arteries.
EDHF-type relaxation in mesenteric arteries isolated from A, normal, B, diabetic, C, normal+DiOHF, D, diabetic+DiOHF rats. In each group of experiments, arteries were precontracted with phenylephrine to similar level: A, 62±3, B, 63±4, C, 63±4, D, 61±2%KPSS, n = 5–12 experiments. Results are shown as mean±SEM. See Table 2 for values.
Figure 5.
Western blot analysis of protein expression.
Western blot of A, eNOS (130 kDa), B, eNOS dimers and monomers (260 kDa) and C, Nox2 (58 kDa) in the normal and diabetic mesenteric arteries with or without DiOHF treatment. Diabetes significantly reduced the expression of eNOS and decreased the proportion of eNOS expressed as the dimer, and increased the expression of Nox2. Treatment with DiOHF significant increased the expression of eNOS, decreased the expression of Nox2 and increased the proportion of eNOS expressed as the dimer. Representative blots were shown on each corresponding graphs. n = 5–6 experiments. Results are shown as mean±SEM. * p<0.05, ** p<0.01, *** p<0.001.