淫羊藿水抽提物舒張離體大白兔胸主動脈之活性研究

Induction of Vasorelaxation in Isolated Rabbit Aorta by Epimedium Brevicornum Maxim Leaf Extracts

本研究探討淫羊藿水抽提物（water extract of Epimedium brevicornum Maxim; EB-W ）舒張離體大白兔胸主動脈之機轉。結果顯示EB-W 在0.001-1 mg/mL 的濃度範圍內呈現劑量相關性地拮抗腎上腺素（phenylephrine ）引起的血管收縮反應。此血管舒張反應可以明顯地，但不完全地，因為去除血管內膜、 預處理NG-nitro-L-arginine methyl ester ）一氧化氮合成{^FA5B^} 抑制劑）及1-H-[1,2,4] oxadiazolo[4, 3-α]quinoxalin-1-one （guanylate cyclase 抑制劑）而受到抑制，顯示EBW 透過部份內膜依賴性的機轉產生舒張血管活性。而EB-W 在去除內膜血管的殘餘舒張反應可因為曝露於高鉀（60 mM KCl ）溶液中及預處理ATP- 敏感性的鉀離子通道阻斷劑（glibenclamide ）而完全被抑制。綜合以上結果顯示淫羊藿水抽提物可透過刺激血管內膜釋放一氧化氮及活化血管平滑肌上的ATP- 敏感性鉀離子通道而產生舒張活性。The vasorelaxant effect of Epimedium brevicornum Maxim (Berberidaceae) (EB) was studied in isolated rabbit thoracic aorta. Results showed that water extract of EB (EB-W) concentration-dependently antagonized phenylephrine (PE)-induced vasoconstriction at the concentrations ranging from 0.001 to 1 mg/mL with an EC50 of 12.4 ± 1.5 μg/mL. EB-W evoked vasorelaxation was significantly, however, not completely inhibited by endothelium removal, NG-nitro- L-arginine methyl ester (a nitric oxide synthase inhibitor) and 1-H-[1,2,4] oxadiazolo [4, 3-α] quinoxalin-1-one (a guanylate cyclase inhibitor) pretreatment, indicated that this vasorelaxant effect to be mediated partially through endothelium-dependent mechanism. The residue relaxation caused by EB-W in PE-precontracted endothelium-denuded preparations was abolished in the presence of high extracellular K+ concentration (60 mM) and by an ATPsensitive K+ channel blocker glibenclamide pretreatment. Taken together, these results suggested that E. brevicornum may relax vascular beds via both direct NO releasing effect from endothelium and activation of an ATP- sensitive K+ channel on smooth muscle.