Matsuura M, Kimura Y, Nakata K, Baba K, Okuda H
Second Department of Medical Biochemistry, School of Medicine, Ehime University, Ehime, Japan.
Planta Med. 2001 Apr;67(3):230-5. doi: 10.1055/s-2001-12011.
An EtOAc-soluble fraction from a 50% EtOH extract of the roots of Angelica keiskei inhibited phenylephrine-induced vasoconstriction in rat aortic rings, while an EtOAc-insoluble fraction had no effect at 100 micrograms/ml. Five active substances isolated from the EtOAc-soluble fraction of the roots were identified as xanthoangelol (1), 4-hydroxyderricin (2), and xanthoangelols B (3), E (4) and F (5), which inhibited phenylephrine-induced vasoconstriction at the concentrations of 10-100 micrograms/ml. It was found that xanthoangelol (1), 4-hydroxyderricin (2), and xanthoangelols E (4) and F (5) inhibited the phenylephrine-induced vasoconstriction through endothelium-dependent endothelium-derived relaxing factor (EDRF) production and/or nitric oxide (NO) production. Among the five chalcones, xanthoangelol B (3) inhibited the phenylephrine-induced vasoconstriction most strongly, and it inhibited the phenylephrine-induced vasoconstriction in the presence or absence of endothelium and in the presence or absence of NG-monomethyl-L-arginine (L-NMMA) (an NO synthetase inhibitor). Furthermore, 4-hydroxyderricin (2) and xanthoangelol B (3) at concentrations of 10-100 micrograms/ml concentration-dependently inhibited the elevation of intracellular free calcium [Ca2+]i induced by phenylephrine. These results demonstrate that compounds 1, 2, 4 and 5 inhibit phenylephrine-induced vasoconstriction through endothelium-dependent production of EDRF/NO and/or through the reduction of the [Ca2+]i elevation induced by phenylephrine. On the other hand, the inhibitory mechanism of compound 3 on phenylephrine-induced vasoconstriction might involve the direct inhibition of smooth muscle functions through the reduction of [Ca2+]i elevation without affecting EDRF/NO production.
当归（Angelica keiskei）根的50%乙醇提取物中的乙酸乙酯可溶部分抑制了苯肾上腺素诱导的大鼠主动脉环血管收缩，而乙酸乙酯不溶部分在100微克/毫升时无作用。从根的乙酸乙酯可溶部分分离出的五种活性物质被鉴定为黄当归醇（1）、4-羟基德里辛（2）、黄当归醇B（3）、E（4）和F（5），它们在10-100微克/毫升的浓度下抑制了苯肾上腺素诱导的血管收缩。研究发现，黄当归醇（1）、4-羟基德里辛（2）、黄当归醇E（4）和F（5）通过内皮依赖性内皮衍生舒张因子（EDRF）产生和/或一氧化氮（NO）产生来抑制苯肾上腺素诱导的血管收缩。在这五种查耳酮中，黄当归醇B（3）对苯肾上腺素诱导的血管收缩抑制作用最强，并且在有或无内皮以及有或无NG-单甲基-L-精氨酸（L-NMMA，一种NO合酶抑制剂）存在的情况下均能抑制苯肾上腺素诱导的血管收缩。此外，浓度为10-100微克/毫升的4-羟基德里辛（2）和黄当归醇B（3）浓度依赖性地抑制了苯肾上腺素诱导的细胞内游离钙[Ca2+]i升高。这些结果表明，化合物1、2、4和5通过内皮依赖性EDRF/NO产生和/或通过降低苯肾上腺素诱导的[Ca2+]i升高来抑制苯肾上腺素诱导的血管收缩。另一方面，化合物3对苯肾上腺素诱导的血管收缩的抑制机制可能涉及通过降低[Ca2+]i升高直接抑制平滑肌功能，而不影响EDRF/NO产生。
