辛夷二氯甲烷提取物对离体大鼠胸主动脉环的舒张作用及其机制  

Vasodilatatory effect and mechanism of CH_2Cl_2 extract of flos magnoliae on isolated rat thoracic aorta

作　　者：张洪平[1] 李亚娟[1] 章丹丹[1] 卞卡[1,2,3] 

机构地区：[1]上海中医药大学穆拉德中药现代化研究中心 [2]上海教委一氧化氮和炎症医学E-研究院,上海201203 [3]德克萨斯大学休斯顿医学院综合生物及药理学系,德克萨斯大学分子医学研究所,休斯顿TX77030

出　　处：《中国病理生理杂志》2010年第9期1689-1694,共6页Chinese Journal of Pathophysiology

基　　金：国家科技部“十一五”支撑计划资助项目(No2006BAI11B08-03);上海市教委高校一氧化氮与炎症医学E研究院计划资助项目(NoE-04010);国家科技重大专项重大新药创制资助项目(No2009ZX09311-003);上海市科委中药现代化专项资助项目(No08DZ1972104)

摘　　要：目的:研究辛夷二氯甲烷提取物(CEF)的舒张血管作用以及其作用机制。方法:采用大鼠离体血管功能实验装置,描记张力变化,每组血管来自5只同批大鼠,分别保留和去除内皮。结果:CEF(0.1-1000mg/L)对去氧肾上腺素(PE)预收缩的血管环具有浓度依赖的舒张作用,内皮去除前后最大舒张效率Emax分别为78.68%±6.03%和64.98%±13.90%,该舒张作用为非内皮依赖性(P<0.05)。钾通道阻断剂格列苯脲(Glib,10μmol/L)、四乙基氯化铵(TEA,3mmol/L)、氯化钡(BaCl2,100μmol/L)和鸟苷酸环化酶抑制剂1H-[1,2,3]恶二唑[4,3-a]喹喔啉-1-酮(ODQ,10μmol/L)预处理不能抑制CEF对去除内皮血管的舒张效应;CEF对血管紧张素Ⅱ(AngⅡ)、前列腺素F2α(PGF2α)、多巴胺(Dopa)、血管加压素(Vaso)、五羟色胺(5-HT)和PE诱发的血管收缩均具有明显的抑制作用(P<0.01),抑制率分别为91.31%、82.11%、95.32%、90.53%、72.22%和83.63%。CEF对无钙液中PE引起的内钙释放和无钙高钾液中Ca2+收缩曲线均有显著的抑制作用(P<0.01)。结论:CEF具有舒张血管作用,其机制可能与抑制外钙内流和胞质内钙释放干扰胞质内钙离子平衡有关。AIM： To characterize the vasodilatatory effect of CH2Cl2 extract of flos magnoliae （ CEF） on isolated rat thoracic aorta and to elucidate its possible mechanism. METHODS： The thoracic aorta was isolated from male Sprague-Dawley （ SD） rats and the isometric tension of aortic rings with or without endothelium was measured. RESULTS： CEF （ 0. 1-1 000 mg/L） produced concentration-dependent,endothelium-independent relaxations in phenylephrine （ PE）-contracted aortic rings. The maximum relaxation induced by CEF was 78. 68% ± 6. 03% in endothelium intact rings and 64. 98% ± 13. 90% in endothelium removed rings while the forskolin （ 1 μmol/L）-induced vasodilation was obtained as 100% . The vasodilatatory effect of CEF was not statistically inhibited by 10 μmol/L glibenclamide （ Glib） ,3 mmol/L tetraethylammonium （ TEA） ,100 μmol/L BaCl2 and 10 μmol/L 1H-[1,2,4]-oxadiazole-[4,3a]-quinoxalin-1-one （ ODQ） in the preparations without endothelium. The CEF pre-treatment significantly inhibited vasoconstrictions to angiotensin Ⅱ （ AngⅡ） ,prostaglandin F2α,（ PGF2α） ,dopamine （ Dopa） ,vasopressin （ Vaso） ,5hydroxytryptamine （ 5-HT） and PE by 91. 31% ,82. 11% ,95. 32% ,90. 53% ,72. 22% and 83. 63% ,respectively（ P 0. 01） . In Ca2＋-free medium treated endothelium removed aortic ring,incubation with CEF at concentration of 82 mg/L significantly attenuated intracellular Ca2 ＋ release by PE. In Ca2 ＋-free ＋ high potassium medium incubated aortic rings without endothelium,CEF （ 82 mg/L） markedly inhibited potassium-stimulated Ca2 ＋-dependent contraction which was mainly due to Ca2 ＋ influx （ P 0. 01） . CONCLUSION： CEF induced vasorelaxation is mainly related to interfering intracellular calcium homeostasis by blocking Ca2 ＋ influx and intracellular Ca2 ＋ release.

关 键 词：血管舒张 辛夷 钙通道 

分 类 号：R54[医药卫生—心血管疾病]