中国药师
中國藥師
중국약사
CHINA PHARMACIST
2015年
6期
884-887
,共4页
复方夏枯草提取物%胸主动脉%血管舒张作用
複方夏枯草提取物%胸主動脈%血管舒張作用
복방하고초제취물%흉주동맥%혈관서장작용
Active fraction from compound Prunella vulgaris L.%Thoracic aorta%Vasodilator effect
目的：：探讨复方夏枯草活性部位( AFCP)对大鼠离体胸主动脉的作用及其可能的机制。方法：采用离体大鼠胸主动脉张力实验,经生物信号采集与分析系统测定血管环张力的变化,观察AFCP的舒张血管作用。结果：AFCP(100~500μg·ml-1)能显著降低苯肾上腺素(PE,1μmol·L-1)引起的血管收缩,对内皮完整和去内皮血管均有(75%±8%)舒张作用。 AFCP的舒血管作用不受一氧化氮合酶抑制药L-NNA、岛苷酸环化酶抑制药MB、钾通道阻滞药TEA和格列苯脲的影响。在无钙K-H 液中AFCP(300μg·ml-1)可使CaCl2的量效曲线下移且使PE的最大收缩幅度降低。结论：AFCP够浓度依赖性舒张大鼠胸主动脉,其舒张血管作用无内皮依赖性。其作用机制可能与抑制细胞内钙离子释放和细胞外钙离子内流有关,与NO途径、前列环素生成和钙激活的钾通道无关。
目的：：探討複方夏枯草活性部位( AFCP)對大鼠離體胸主動脈的作用及其可能的機製。方法：採用離體大鼠胸主動脈張力實驗,經生物信號採集與分析繫統測定血管環張力的變化,觀察AFCP的舒張血管作用。結果：AFCP(100~500μg·ml-1)能顯著降低苯腎上腺素(PE,1μmol·L-1)引起的血管收縮,對內皮完整和去內皮血管均有(75%±8%)舒張作用。 AFCP的舒血管作用不受一氧化氮閤酶抑製藥L-NNA、島苷痠環化酶抑製藥MB、鉀通道阻滯藥TEA和格列苯脲的影響。在無鈣K-H 液中AFCP(300μg·ml-1)可使CaCl2的量效麯線下移且使PE的最大收縮幅度降低。結論：AFCP夠濃度依賴性舒張大鼠胸主動脈,其舒張血管作用無內皮依賴性。其作用機製可能與抑製細胞內鈣離子釋放和細胞外鈣離子內流有關,與NO途徑、前列環素生成和鈣激活的鉀通道無關。
목적：：탐토복방하고초활성부위( AFCP)대대서리체흉주동맥적작용급기가능적궤제。방법：채용리체대서흉주동맥장력실험,경생물신호채집여분석계통측정혈관배장력적변화,관찰AFCP적서장혈관작용。결과：AFCP(100~500μg·ml-1)능현저강저분신상선소(PE,1μmol·L-1)인기적혈관수축,대내피완정화거내피혈관균유(75%±8%)서장작용。 AFCP적서혈관작용불수일양화담합매억제약L-NNA、도감산배화매억제약MB、갑통도조체약TEA화격렬분뇨적영향。재무개K-H 액중AFCP(300μg·ml-1)가사CaCl2적량효곡선하이차사PE적최대수축폭도강저。결론：AFCP구농도의뢰성서장대서흉주동맥,기서장혈관작용무내피의뢰성。기작용궤제가능여억제세포내개리자석방화세포외개리자내류유관,여NO도경、전렬배소생성화개격활적갑통도무관。
Objective:To investigate the vasorelaxant effect of active fraction from compound Prunella vulgaris L. ( AFCP) on the i-solated thoracic aorta of rats and underlying mechanism. Methods:The study was performed with the tension experiment of the isolate rat thoracic aorta. The changes of vascular ring tension were measured by biological signal acquisition and analysis system, and the vasodila-tor effect of AFCP was observed. Results:AFCP(100-500μg·ml-1)could induce significant relaxation in aorta rings pre-contracted by phenylephrine (PE,1 μmol·L-1), and the relaxation effect was significant(75% ±8%) in endothelium-intact aortic and endothelium-denuded aortic. The vasodilatation effect of AFCP was not significantly affected by nitric oxide synthase ( NOS) inhibitor NG-nitro-L-argi-nine( L-NNA) , guanylate cyclase inhibitor MB,potassium channel blocker TEA and glibenclamide. In Ca2+-free bath solutions, AFCP (300 μg·ml-1 ) could shift downward dose-response curve of CaCl2 and significantly reduce the maximum contraction amplitude of PE. Conclusion:AFCP can relax rat aorta rings in a dose-dependent manner, which is endothelium-independent. The mechanism may be re-lated to the inhibition of intracellular calcium release and extracellular calcium flow, and has nothing to do with NO pathway, prostacyclin generation and calcium-activated potassium channels.
