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鬼箭羽 부탄올 추출물의 혈관이완 기전에 대한 연구

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

이호섭|강대길|이준경|김승주|이계복|최호진|리향|최덕호|염기복
한의병리학회 (The Society of Pathology in Korean Medicine)|2008.02|동의생리병리학회지 (Journal of Physiology & Pathology in Korean Medicine)|제22권 제1호|pp. 148-154

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참고문헌

키워드

relaxationendotheliumbutanol extracts of Euonymus alatus (BEA)aortic tissuesnitric oxide/cGMP signaling
주제분류한의학

초록

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 NG-nitro-L-arginine methylester (L-NAME), and 1 H-[1,2,4]-oxadiazole- [4,3-α]-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.

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 NG-nitro-L-arginine methylester (L-NAME), and 1 H-[1,2,4]-oxadiazole- [4,3-α]-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.

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