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Updated: Aug 31, 2026

Preparation of Washed Human Platelets for Quantitative Metabolic Flux Studies
Published on: January 10, 2025
The role of polyphenolic compounds in the diet as inhibitors of platelet function
Gary P Hubbard1, Siegfried Wolffram, Julie A Lovegrove
1School of Food Biosciences, University of Reading, Whiteknights, Reading, Berks, RG6 6AL, UK. g.p.hubbard@reading.ac.uk
Insights
Dietary polyphenols, like quercetin, show potential in inhibiting platelet activation, a key factor in cardiovascular disease. However, current dietary interventions did not significantly alter platelet aggregation in vivo.
Area of Science:
- Cardiovascular disease research
- Dietary interventions and health
Background:
- Platelets are crucial in cardiovascular disease development.
- Dietary components like polyphenols are investigated for their anti-platelet effects.
- Antioxidants, including polyphenols from fruits and vegetables, can inhibit platelet function.
Purpose of the Study:
- To investigate the in vitro effects of hydroxycinnamates and quercetin on platelet activation and signaling.
- To examine the in vivo effects of a polyphenol-rich diet on platelet aggregation.
Main Methods:
- In vitro studies on platelet activation and cell signaling pathways.
- In vivo study with 20 subjects on a low-polyphenol diet followed by polyphenol-rich meals for 5 days.
- Measurement of platelet aggregation and plasma flavonols at baseline and after intervention.
Main Results:
- Hydroxycinnamates inhibited platelet function in vitro, but not at achievable dietary levels.
- Quercetin demonstrated significant inhibition of platelet aggregation, intracellular calcium mobilization, and tyrosine phosphorylation in vitro.
- Plasma flavonoid levels increased significantly after dietary intervention (P = 0.001).
- No significant changes in ex vivo platelet aggregation were observed after the 5-day intervention.
Conclusions:
- Quercetin shows promise as an inhibitor of platelet activation in vitro.
- Dietary polyphenol interventions require further investigation to demonstrate in vivo efficacy in reducing platelet aggregation.
- Individual polyphenol effects on platelet function need further study to clarify their role in cardiovascular disease risk.
Abstract:
Platelets play a substantial role in cardiovascular disease, and for many years there has been a search for dietary componentsthat are able to inhibit platelet function and therefore decrease the risk of cardiovasculardisease. Platelets can be inhibited by alcohol, dietary fats and some antioxidants, including agroup of compounds, the polyphenols, found in fruits and vegetables. A number of these compounds have been shown to inhibit platelet function both in vitro and in vivo. In the present study the effects of the hydroxycinnamates and the flavonoid quercetin on platelet activation and cell signalling in vitro were investigated. The hydroxycinnamates inhibited platelet function, although not at levels that can be achieved in human plasma by dietary intervention. However, quercetin inhibited platelet aggregation at levels lower than those previously reported. Quercetin was also found to inhibit intracellular Ca mobilisation and whole-cell tyrosine protein phosphorylation in platelets, which are both processes essential for platelet activation. The effect of polyphenols on platelet aggregation in vivo was also investigated. Twenty subjects followed a low-polyphenol diet for 3 d before and also during supplementation. All subjects were supplemented with a polyphenol-rich meal every lunchtime for 5d. Platelet aggregation and plasma flavonols were measured at baseline and after 5d of dietary supplementation. Total plasma flavonoids increased significantly after the dietary intervention period (P = 0.001). However, no significant changes in ex vivo platelet aggregation were observed. Further investigation of the effects of individual polyphenolic compoundson platelet function, both in vitro and in vivo, is required in order to elucidate their role in the relationship between diet and the risk of cardiovascular disease.
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