Extracts of feverfew may inhibit platelet behaviour via neutralization of sulphydryl groups.
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.
D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism*; D001797:Blood Protein Electrophoresis; D003545:Cysteine / Q000494:pharmacology; D006801:Humans; D066298:In Vitro Techniques; D007202:Indicators and Reagents; D010936:Plant Extracts / Q000494:pharmacology; D010946:Plants, Medicinal / Q000032:analysis*; D010974:Platelet Aggregation / Q000187:drug effects; D012717:Sesquiterpenes / Q000494:pharmacology; D013438:Sulfhydryl Compounds / Q000097:blood*
D001095:Arachidonic Acids; D007202:Indicators and Reagents; D010936:Plant Extracts; D012717:Sesquiterpenes; D013438:Sulfhydryl Compounds; D016718:Arachidonic Acid; C002669:parthenolide; D003545:Cysteine