Extracts of feverfew may inhibit platelet behaviour via neutralization of sulphydryl groups

J Pharm Pharmacol. 1987 Jun;39(6):459-65. doi: 10.1111/j.2042-7158.1987.tb03420.x.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Arachidonic Acid
  • Arachidonic Acids / metabolism
  • Blood Platelets / drug effects
  • Blood Platelets / metabolism*
  • Blood Protein Electrophoresis
  • Cysteine / pharmacology
  • Humans
  • In Vitro Techniques
  • Indicators and Reagents
  • Plant Extracts / pharmacology
  • Plants, Medicinal / analysis*
  • Platelet Aggregation / drug effects
  • Sesquiterpenes / pharmacology
  • Sulfhydryl Compounds / blood*

Substances

  • Arachidonic Acids
  • Indicators and Reagents
  • Plant Extracts
  • Sesquiterpenes
  • Sulfhydryl Compounds
  • Arachidonic Acid
  • parthenolide
  • Cysteine