Blood vessels, thrombosis & hemostasis · 2026
New insights into flavonoid binding to the thromboxane A2 receptor.
СтатьяНазвание и аннотация: Перевод в очереди
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Han Chao, Chu Xiang, Ren Pengxuan, Lonkar Payal, Bassot Arthur, Cosset Erika, Xu Bin, Mammadova-Bach Elmina, Gudermann Thomas, Braun Attila
Аннотация
Aspirin treatment irreversibly inhibits cyclooxygenase activity, blocking thromboxane A2 (TxA2) synthesis and reducing thromboxane-prostanoid (TP) receptor-induced platelet activation. Aspirin resistance refers to the failure of regular aspirin doses to produce the expected antiplatelet effect. Aspirin-induced bleeding complications are frequently observed in patients receiving excessive doses or combined antiplatelet and anticoagulant therapy. Although selective TP receptor antagonists have been tested clinically, they are ineffective due to persistently high prostaglandin levels, causing unexpected signaling effects in platelets and other cell types. Hydroxyflavonoids are bioactive phytonutrients with antithrombotic effects, inhibiting TxA2-mediated platelet signaling and preventing abnormal platelet activation in cardiovascular diseases without major side effects. Using a recently published TP receptor crystal structure and docking studies with different flavonoid classes, including genistein and tectorigenin, we found that flavonoids occupy similar ligand-binding surface of TxA2, thereby preventing TxA2 binding. To evaluate our bioinformatics data, a mutant TP receptor variant was overexpressed in HEK293 cells, deleting interacting amino acids with hydroxyflavonoids, and stimulated with the TxA2 analog U46619. Intracellular Ca2+ responses were measured in Fura-2-labeled cells. Amino acid substitutions in the extracellular domain, which did not influence U46619 binding, abolished hydroxyflavonoid-mediated inhibition of the TP receptor. These results suggest that hydroxyflavonoids directly bind to and inhibit the TP receptor. Using aggregometry and flow chamber assays, we confirmed that genistein and tectorigenin synergize with aspirin to inhibit platelet aggregation and thrombus growth in human and mouse platelets. Whether combined genistein-aspirin therapy improves antiplatelet responses in aspirin-resistant patients requires further investigation.