Key result
Luteolin inhibits collagen-induced platelet aggregation with an IC50 of ~28 µM via PI3K/Akt and MAPK pathways.
Why the study?
Platelet hyperactivation and aggregation contribute critically to thrombotic events, and natural flavonoids like luteolin may modulate platelet function but require mechanistic investigation.
Answers are grounded in this paper and cite their sources.
Should not change antiplatelet practice; leaves open luteolin's antithrombotic potential for in vivo validation.
Cardiovascular diseases are the leading cause of death worldwide, with platelet hyperactivation and aggregation being critical contributors to thrombotic events.Natural flavonoids have gained attention for their potential in modulating platelet function.This study investigated the antiplatelet effects of luteolin, a dietary flavone abundant in celery, parsley, and chamomile, and its underlying molecular mechanisms.Using in vitro platelet function assays, we demonstrated that luteolin significantly inhibited collagen-induced platelet aggregation in a concentrationdependent manner.Luteolin suppressed serotonin release and intracellular Ca 2+ mobilization, while attenuating thromboxane B 2 production.Furthermore, Western blot analysis revealed that luteolin inhibited phosphorylation of key signaling molecules, including phosphatidylinositol 3-kinase/protein kinase B and Mitogen-Activated Protein Kinase.These findings suggest that luteolin exerts its antiplatelet activity by targeting multiple signaling pathways involved in platelet activation.Taken together, our results highlight luteolin as a promising natural flavonoid with potential therapeutic applications in the prevention and treatment of thrombotic cardiovascular diseases.
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Park et al. (2025) studied Platelet hyperactivation and aggregation (in vitro). Luteolin vs. Collagen-induced platelets (vehicle control) was evaluated on Collagen-induced platelet aggregation (IC50 27.97 µM, p=<0.001). Luteolin significantly inhibited collagen-induced human platelet aggregation in a concentration-dependent manner with an IC50 of 27.97 µM by modulating PI3K/Akt and MAPK signaling pathways.
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