Methods Platelet aggregation was performed by light-transmission aggregometry. Fibrinogen-binding and P-Selectin exposure were measured by flow cytometry.

Results Consistent with previous studies, quercetin inhibited collagen-stimulated (5 µg/ml) platelet aggregation in a dose-dependent manner; significant inhibition was observed as low as 3 µM (lower than previously reported). Above 6 µM, aggregation was inhibited >90%. In-vivo, numerous agonists are present at lower concentrations than typically used in in-vitro assays. Agonist concentrations that individually are subthreshold for aggregation, when added together, may synergise and stimulate substantial functional responses. The ability and potency of quercetin to inhibit fibrinogen-binding to platelets stimulated by this synergistic response between thrombin and CRP (Collagen-Related-Peptide) was therefore explored. Quercetin inhibited significantly fibrinogen-binding at concentrations as low as 500 nM. This was associated with substantial inhibition of alpha-granule secretion. Fibrinogen-binding and P-Selectin exposure stimulated by 0.1 µg/ml and 1 µg/ml CR P alone was also significantly inhibited by quercetin, at concentrations as low as 500 nM.

Conclusions Quercetin inhibits platelet function at concentrations lower than previously recognised and within potential physiological concentrations. Development of this work will allow elucidation and modelling of the effects of quercetin's main metabolites.