木犀草素对大鼠主动脉的舒张作用及相关机制研究  

Vasodilation effect of luteolin on rat thoracic aorta and its mechanism

作　　者：蒋惠娣[1] 汝海龙[1] 王霄霞[1] 夏强[2] 屠洁[2] 

机构地区：[1]浙江大学药学院,浙江杭州310031 [2]浙江大学医学院,浙江杭州310031

出　　处：《中国药学杂志》2005年第6期427-430,共4页Chinese Pharmaceutical Journal

基　　金：浙江省中医药局(G20010358)浙江省科技厅重点资助项目(C20020578)

摘　　要：目的观察木犀草素的舒血管作用并探讨其作用机制。方法大鼠胸主动脉环张力测定法。结果在内皮完整及去内皮血管上,木犀草素均浓度(4.5-36 μmol·L-1)依赖性地降低苯肾上腺素(PE)预收缩血管的张力,拮抗高钾引起的血管收缩;木犀草素使PE收缩曲线非平行右移,且使最大张力减小;L-NAME,propranolol对木犀草素的舒血管作用无显著影响;钾通道阻断剂TEA,4-AP,BaCl2,5-HD均能显著减弱木犀草素的血管舒张作用;木犀草素可以显著地对抗无钙、无钾、无钙环境下渐复钙后由PE引起的血管收缩。结论木犀草素对血管的舒张作用表现为非内皮依赖性,其舒张作用与其直接抑制电压依从性钙通道、受体操纵性钙通道、细胞内钙释放,以及激活钾通道有关,而与α,β受体无关。OBJECTIVE: To investigate the vasodilation effect and underlying mechanism of luteolin. METHODS: The tension of rat thoracic aorta rings was measured. RESULTS: Luteolin (4.5-36 μmol&middotL-1) caused the concentration-dependent relaxation of endothelium-intact or endothelium-denuded aorta rings precontracted with phenylephrine (PE,10 -6mol&middotL-1) and high level of K+ (6 × 10-2 mol&middotL-1). Luteolin caused unparallel shift of the PE concentration-response curve to the right, reduced the maximal contraction induced by PE. L-NAME and propranolol did not affect the effect of luteolin on rat thoracic aorta rings, however 5-hydroxydecanoate, tetraethylammonium, BaCl2 and 4-aminopyridine reduced the vasodilation effect of luteolin significantly. Luteolin obviously reduced PE induced transient contraction in Ca2+-free medium and K +-free solution, and PE induced contraction after steady contraction in free Ca2+ solution. CONCLUSION: Luteolin induced endothelium-independent relaxation in rat thoracic aorta. The mechanism was related to the inhibition of voltage-dependent Ca2+ channel (VDC), receptor-operate Ca2+ channel (ROC), the release of intracellular Ca2+ and the activation of K+ channel. α and β-adrenoceptor were not involved in its relaxation.

关 键 词：木犀草素 血管 舒张 机制 

分 类 号：R965[医药卫生—药理学]