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Study on the Vasorelaxant Mechanism of the Butanol Extract of Euonymus alatus  

Li, Xiang (Professional Graduate School of Oriental Medicine, Wonkwang University)
Kang, Dae-Gill (Professional Graduate School of Oriental Medicine, Wonkwang University)
Lee, Jun-Kyoung (Professional Graduate School of Oriental Medicine, Wonkwang University)
Kim, Seung-Ju (Korea Institute of Oriental Medicine)
Choi, Deok-Ho (Professional Graduate School of Oriental Medicine, Wonkwang University)
Lee, Kye-Bok (Professional Graduate School of Oriental Medicine, Wonkwang University)
Cui, Hao-Zhen (Professional Graduate School of Oriental Medicine, Wonkwang University)
Yeom, Ki-Bok (Professional Graduate School of Oriental Medicine, Wonkwang University)
Lee, Ho-Sub (Professional Graduate School of Oriental Medicine, Wonkwang University)
Publication Information
Journal of Physiology & Pathology in Korean Medicine / v.22, no.1, 2008 , pp. 148-154 More about this Journal
Abstract
The butanol extract of Euonymus alatus (BEA) induced dose-dependent relaxation of phenylephrine-precontracted aorta, which was abolished by removal of functional endothelium. Pre-treatment of the endothelium-intact aortic tissues with $N^G-nitro-L-arginine methylester$ (L-NAME), and 1 H-[1,2,4]-oxadiazole- [$4,3-{\alpha}$]-quinoxalin-1-one (ODQ) inhibited the relaxation induced by BEA, respectively. BEA-induced vascular relaxation was not blocked by glibenclamide, tetraethylammonium (TEA), indomethacin, atropine, propranolol, verapamil, and diltiazem, respectively. Moreover, BEA inhibits phenylephrine-induced vascular constriction in a dose-dependent manner. These results suggest that BEA relaxes vascular smooth muscle via endothelium-dependent nitric oxide/cGMP signaling.
Keywords
butanol extracts of Euonymus alatus (BEA); aortic tissues; endothelium; nitric oxide/cGMP signaling; relaxation;
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