title: Ingestion of quercetin inhibits platelet aggregation and essential components of the collagen-stimulated platelet activation pathway in humans.
abstract: BACKGROUND
  Quercetin, a flavonoid present in the human diet, which is found in high levels in onions, apples, tea and wine, has been shown previously to inhibit platelet aggregation and signaling in vitro. Consequently, it has been proposed that quercetin may contribute to the protective effects against cardiovascular disease of a diet rich in fruit and vegetables.
  
  
  OBJECTIVE
  A pilot human dietary intervention study was designed to investigate the relationship between the ingestion of dietary quercetin and platelet function.
  
  
  METHODS
  Human subjects ingested either 150 mg or 300 mg quercetin-4'-O-beta-D-glucoside supplement to determine the systemic availability of quercetin. Platelets were isolated from subjects to analyse collagen-stimulated cell signaling and aggregation.
  
  
  RESULTS
  Plasma quercetin concentrations peaked at 4.66 microm (+/- 0.77) and 9.72 microm (+/- 1.38) 30 min after ingestion of 150-mg and 300-mg doses of quercetin-4'-O-beta-D-glucoside, respectively, demonstrating that quercetin was bioavailable, with plasma concentrations attained in the range known to affect platelet function in vitro. Platelet aggregation was inhibited 30 and 120 min after ingestion of both doses of quercetin-4'-O-beta-D-glucoside. Correspondingly, collagen-stimulated tyrosine phosphorylation of total platelet proteins was inhibited. This was accompanied by reduced tyrosine phosphorylation of the tyrosine kinase Syk and phospholipase Cgamma2, components of the platelet glycoprotein VI collagen receptor signaling pathway.
  
  
  CONCLUSIONS
  This study provides new evidence of the relatively high systemic availability of quercetin in the form of quercetin-4'-O-beta-D-glucoside by supplementation, and implicates quercetin as a dietary inhibitor of platelet cell signaling and thrombus formation.
authors.affiliation: School of Food Biosciences, University of Reading, Reading, UK.
authors.forename: G P
authors.initials: GP
authors.lastname: Hubbard
authors.forename: S
authors.initials: S
authors.lastname: Wolffram
authors.forename: J A
authors.initials: JA
authors.lastname: Lovegrove
authors.forename: J M
authors.initials: JM
authors.lastname: Gibbins
mesh_terms: D001792:Blood Platelets / Q000187:drug effects; D002318:Cardiovascular Diseases / Q000517:prevention & control; D002851:Chromatography, High Pressure Liquid; D003094:Collagen / Q000378:metabolism*; D018592:Cross-Over Studies; D019587:Dietary Supplements; D004305:Dose-Response Relationship, Drug; D005260:Female; D044948:Flavonols / Q000494:pharmacology; D005960:Glucosides / Q000737:chemistry; D006801:Humans; D015151:Immunoblotting; D008297:Male; D010766:Phosphorylation; D015539:Platelet Activation / Q000187:drug effects*; D010974:Platelet Aggregation / Q000187:drug effects*; D011794:Quercetin / Q000031:analogs & derivatives* / Q000494:pharmacology*; D015398:Signal Transduction; D013927:Thrombosis / Q000378:metabolism; D013997:Time Factors; D014443:Tyrosine / Q000378:metabolism
chemical_list: D044948:Flavonols; D005960:Glucosides; C405012:tamarixetin 3-O-neohesperidoside; C047368:3-methylquercetin; D014443:Tyrosine; D003094:Collagen; D011794:Quercetin; C080613:spiraeoside