Key result
Quercetin inhibits human platelet function by blocking signaling molecules and granule exocytosis.
Why the study?
The lowest quercetin concentration that significantly inhibits agonist-induced platelet aggregation remains contradictory, and its inhibitory effects on human platelet function require clarification.
Does quercetin inhibit human platelet function?
Does quercetin inhibit human platelet function?
Quercetin exerts broad antiplatelet effects by inhibiting aggregation, granule exocytosis, and key intracellular signaling kinases.
Should not yet alter antiplatelet strategies; leaves open clinical translation pending dose-finding studies.
Quercetin (Que) is one of the most abundant and potent naturally occurring antioxidant. Que has been shown to exert many biological activities, including antiplatelet activity. Indeed, Que was shown to inhibit platelet aggregation in response to platelet agonists, such as ADP, collagen, thrombin and arachidonic acid. However, the lowest Que concentration that significantly inhibits agonist-induced platelet aggregation remains contradictory. In addition, to anti-aggregatory effects, Que was demonstrated to inhibit platelet dense and alpha granule exocytosis when stimulated by different platelet agonists. Que was also shown to inhibit multiple platelet protein kinases, including, PI3K, Akt, PLC and PKC. The main aim of this review focuses on the inhibitory effects of Que on human platelet function.
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Sapha Mosawy (2015) conducted a review in Platelet aggregation and thrombosis. Quercetin was evaluated. Quercetin inhibits human platelet function via multiple mechanisms, including the inhibition of signaling molecules and granule exocytosis, though the lowest effective concentration remains unclear.
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