Anti-thrombotic Effects of Apigenin Through Regulation of Phosphoprotein and Granule Secretion in Human Platelets

Cardiovascular disease is a major health problem worldwide, and excessive platelet activation and aggregation are identified as the main causes of cardiovascular disease. Therefore, controlling platelet activation is a key strategy in the prevention and treatment of cardiovascular disease. Apigenin is a major flavonoid compound abundantly contained in the flowers of the chamomile plant, and previous studies have reported that it has anti-inflammatory, antiviral, and anticancer effects. However, the efficacy and mechanism of apigenin in inhibiting platelet activation and aggregation have not been clearly elucidated. This study confirmed the effect of apigenin on collagen-induced human platelets and clarified its mechanism of action. Apigenin inhibited the phosphorylation of phosphoproteins PI3K/Akt and MAPK during platelet activation, and also inhibited the phosphorylation of cPLA₂. In addition, apigenin reduced the production of TXA₂ and the release of intraplatelet granules such as ATP and serotonin. As a result, apigenin potently inhibited platelet aggregation induced by collagen, and ultimately affected the inhibition of thrombus formation. Through these results, this study shows that apigenin can be an effective antithrombotic substance that inhibits the activation and aggregation of human platelets by preventing granule release through the regulation of phosphorylated proteins.