Curcumin supplementation could improve diabetes-induced endothelial dysfunction associated with decreased vascular superoxide production and PKC inhibition

<p>Abstract</p> <p>Background</p> <p>Curcumin, an Asian spice and food-coloring agent, is known for its anti-oxidant properties. We propose that curcumin can improve diabetes-induced endothelial dysfunction through superoxide reduction.</p> <p>Methods</p> <p>Diabetes (DM) was induced in rats by streptozotocin (STZ). Daily curcumin oral feeding was started six weeks after the STZ injection. Twelve weeks after STZ injection, mesenteric arteriolar responses were recorded in real time using intravital fluorescence videomicroscopy. Superoxide and vascular protein kinase C (PKC-βII) were examined by hydroethidine and immunofluorescence, respectively.</p> <p>Results</p> <p>The dilatory response to acetylcholine (ACh) significantly decreased in DM arterioles as compared to control arterioles. There was no difference among groups when sodium nitroprusside (SNP) was used. ACh responses were significantly improved by both low and high doses (30 and 300 mg/kg, respectively) of curcumin supplementation. An oxygen radical-sensitive fluorescent probe, hydroethidine, was used to detect intracellular superoxide anion (O₂^●-) production. O₂^●-production was markedly increased in DM arterioles, but it was significantly reduced by supplementation of either low or high doses of curcumin. In addition, with a high dose of curcumin, diabetes-induced vascular PKC-βII expression was diminished.</p> <p>Conclusion</p> <p>Therefore, it is suggested that curcumin supplementation could improve diabetes-induced endothelial dysfunction significantly in relation to its potential to decrease superoxide production and PKC inhibition.</p

The erythrocyte glutathione levels during oral glucose tolerance test

Erythrocytes glutathione (GSH) levels were measured in erythrocytes from 33 subjects, at baseline and after 2-hour glucose loading in order to investigate the effect of glucose ingestion on the erythrocyte GSH. According to the World Health Organisation criteria 18 subjects had normal glucose tolerance (NGT) (mean age 48+/-10 years, 10 women, 8 men), 15 subjects had impaired glucose tolerance (IGT) (mean age 52+/-8 years, 9 women, 6 men). After 12-hour fasting, erythrocyte GSH levels were 40.5+/-8.06 and 39.27+/-10.26 mg/dl hemolisate in subjects with NGT and IGT, respectively (p=N.S). After e-hour glucose loading, erythrocyte GSH levels decreased to 36.01+/-9.4 (p<0.05) and 32.36+/-5.7 (p<0.005) in subjects with NGT and IGT, respectively. The decrease in erythrocyte GSH levels in subjects with IGT was greater than in NGT individuals (p<0.001). There was negative correlation between glucose, insulin, C-peptide, and erythrocyte GSH levels after glucose loading (p<0.005). Our results suggest that glucose loading induce an oxidative stress in all subjects but this oxidative stress is greater in subjects with IGT than with NGT. (C) 1997, Editrice Kurtis