Heptinstall S, Groenewegen W A, Spangenberg P, Loesche W
J Pharm Pharmacol. 1987 Jun;39(6):459-65. doi: 10.1111/j.2042-7158.1987.tb03420.x.
It has been suggested that extracts of feverfew may inhibit platelet behaviour via effects on platelet sulphydryl groups. In the present study we have obtained evidence for such a mode of action. Compounds that contain sulphydryl groups such as cysteine and N-(2-mercaptopropionyl)glycine prevented the inhibition of platelet behaviour by feverfew. Feverfew and parthenolide (one of the active components of feverfew) dramatically reduced the number of acid-soluble sulphydryl groups in platelets. This effect occurred at concentrations similar to those that inhibited platelet secretory activity. Feverfew itself did not induce the formation of disulphide-linked protein polymers in platelets but polymer formation occurred when aggregating agents were added to feverfew-treated platelets. Feverfew evoked changes in the metabolism of arachidonic acid that were similar to those observed in glutathione-depleted platelets.
有人提出，小白菊提取物可能通过对血小板巯基的作用来抑制血小板行为。在本研究中，我们获得了支持这种作用方式的证据。含有巯基的化合物，如半胱氨酸和N-（2-巯基丙酰基）甘氨酸，可防止小白菊对血小板行为的抑制。小白菊和小白菊内酯（小白菊的活性成分之一）显著减少了血小板中酸溶性巯基的数量。这种作用发生的浓度与抑制血小板分泌活性的浓度相似。小白菊本身不会诱导血小板中形成二硫键连接的蛋白质聚合物，但当向经小白菊处理的血小板中添加聚集剂时，会发生聚合物形成。小白菊引起的花生四烯酸代谢变化与在谷胱甘肽缺乏的血小板中观察到的变化相似。
