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


CONCLUSIONS
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.
Inter-Department of Physiology, Graduate School, Chulalongkorn University, Bangkok 10330, Thailand.
Sirada
S
Rungseesantivanon
Naris
N
Thenchaisri
Preecha
P
Ruangvejvorachai
Suthiluk
S
Patumraj
D000109:Acetylcholine; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use*; D001160:Arterioles / Q000187:drug effects / Q000503:physiopathology; D030024:Curcuma / Q000737:chemistry; D003474:Curcumin / Q000494:pharmacology / Q000627:therapeutic use*; D003921:Diabetes Mellitus, Experimental / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism; D019587:Dietary Supplements; D004730:Endothelium, Vascular / Q000187:drug effects*; D005453:Fluorescence; D008297:Male; D009599:Nitroprusside / Q000494:pharmacology; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology / Q000627:therapeutic use*; D011493:Protein Kinase C / Q000037:antagonists & inhibitors; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D013481:Superoxides / Q000378:metabolism*; D014652:Vascular Diseases / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D014661:Vasoconstriction / Q000187:drug effects
D000975:Antioxidants; D010936:Plant Extracts; D017382:Reactive Oxygen Species; D013481:Superoxides; D009599:Nitroprusside; D011493:Protein Kinase C; D003474:Curcumin; D000109:Acetylcholine