Curcuma Longa Abolishes Phenylephrine-Induced Contractions in Isolated Aortic Artery of Rats

Abstract Background: Curcuma longa has biological effects. Its cardiovascular activities are yet to be scientifically studied. Objectives: To investigate the vasorelaxant effects of the aqueous extract of Curcuma longa (AECL). Methods: Aortic annuli of normotensive rats, with or without endothelium, were set up in a data storage system with nutrient solution in recipients, with scientifically recommended temperature, aeration and tension. Over contraction by Phenylephrine, the AECL (1, 3, 10, 30, 100, 300 and 1000 µg/mL) was incubated before and after incubation with atropine or L-name or indomethacin. An AECL concentration-response curve was also built over contractions caused by elevation of extracellular K+. Data were significant when p < 0.05, with GraphPad Prism 6.0 software resolutions. Results: The AECL induced 100% vasorelaxation also in the endothelium-free annuli. The part of the endothelium-dependent effect had EC50 = 4.32 ± 0.05 µg/mL. With inhibition of NO production, the EC50 increased to 126.50 ± 2.35 µg/mL; after inhibition of prostacyclin production, to 124.6 ± 0.05 µg/mL; and after muscarinic blockade, to 437.10 ± 0.2 µg/mL. Opening of K+ channels (relaxation of 56.98%) and VOCC blockade (relaxation of 31.56%) were evident. Conclusion: AECL induced significant vasorelaxation, being more significant in the presence of endothelium. The muscarinic pathway seems to be the main one involved in this effect, followed by the NO production and prostacyclin pathways. The activity in K+ channels by AECL was more significant than its VOCC blockade. The use of other models and tools to study action mechanisms will be important and elucidating.

摘要 背景：姜黄（Curcuma longa）具备多种生物学活性，但其心血管方面的活性尚未经科学探究。
目的：探究姜黄水提物（aqueous extract of Curcuma longa，下文简称AECL）的血管舒张效应。
方法：将带有或去除血管内皮的正常血压大鼠主动脉环安置于装有营养液的器官浴槽中，按照科学推荐的温度、通气条件及肌张力设置进行实验。在经苯肾上腺素（Phenylephrine）预收缩血管环后，分别在阿托品（atropine）、L-名（L-name）或吲哚美辛（indomethacin）孵育的前后，加入浓度为1、3、10、30、100、300及1000 µg/mL的AECL。此外，在细胞外K+浓度升高引发的血管收缩模型上，构建AECL的浓度-反应曲线。采用GraphPad Prism 6.0软件进行数据分析，当p<0.05时认为差异具有统计学意义。
结果：AECL在去除血管内皮的主动脉环上同样可诱导100%的血管舒张。内皮依赖性舒张组分的半数有效浓度（EC50）为4.32±0.05 µg/mL。当一氧化氮（NO）生成受到抑制时，EC50升至126.50±2.35 µg/mL；抑制前列腺环素生成后，EC50升至124.6±0.05 µg/mL；而经毒蕈碱受体阻断后，EC50升至437.10±0.2 µg/mL。实验还观察到，AECL可激活钾离子通道（介导56.98%的舒张效应）并阻断电压门控钙通道（Voltage-Gated Calcium Channels，VOCC），其阻断所致舒张率达31.56%。
结论：AECL可诱导显著的血管舒张效应，且在血管内皮存在时效应更为显著。毒蕈碱通路似乎是介导该血管舒张效应的主要途径，其次为一氧化氮生成通路与前列腺环素通路。AECL对钾离子通道的调控活性强于其对电压门控钙通道的阻断作用。后续采用其他模型与工具探究其作用机制，对于阐明该活性的具体通路具有重要意义。