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

被引:95
作者
Rungseesantivanon, Sirada [2 ]
Thenchaisri, Naris [3 ]
Ruangvejvorachai, Preecha [4 ]
Patumraj, Suthiluk [1 ]
机构
[1] Chulalongkorn Univ, Fac Med, Dept Physiol, Bangkok 10330, Thailand
[2] Chulalongkorn Univ, Grad Sch, Interdept Physiol, Bangkok 10330, Thailand
[3] Kasetsart Univ, Fac Vet Med, Dept Compan Anim Clin Sci, Bangkok 10900, Thailand
[4] Chulalongkorn Univ, Fac Med, Dept Pathol, Bangkok 10330, Thailand
来源
BMC COMPLEMENTARY AND ALTERNATIVE MEDICINE | 2010年 / 10卷
关键词
NITRIC-OXIDE; VITAMIN-C; DEPENDENT VASODILATION; ANTIOXIDANT MECHANISM; OXIDATIVE STRESS; NAD(P)H OXIDASE; INSULIN; ANION; RAT; HYDROETHIDINE;
D O I
10.1186/1472-6882-10-57
中图分类号
R [医药、卫生];
学科分类号
100218 [急诊医学];
摘要
Background: 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. Methods: 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-beta II) were examined by hydroethidine and immunofluorescence, respectively. Results: 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 (O-2(center dot-)) production. O-2(center dot-) 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-beta II expression was diminished. Conclusion: 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.
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页数:9
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