Dihydromyricetin exhibits potent antiplatelet activity with minimal impact on coagulation system: an in vitro study

Plain Language Summary This study aimed to systematically evaluate the antiplatelet activity of dihydromyricetin (DHM) and comprehensively investigate its effects on coagulation function within its therapeutically relevant concentration range. Using in-vitro experiments, we employed a panel of standard assays to assess the effects of DHM on platelet activation and aggregation induced by various agonists [adenosine diphosphate (ADP), arachidonic acid (AA), and collagen (COL)], as well as on agonist-independent adhesion and aggregation. Simultaneously, multidimensional techniques, including conventional coagulation tests, thromboelastography (TEG), and whole-blood dynamic coagulation analysis, were used to systematically evaluate the impact of DHM on the coagulation cascade and overall hemostatic dynamics. The results showed that DHM significantly inhibited platelet activation and aggregation in a concentration-dependent manner and effectively prevented their spontaneous adhesion and aggregation. Crucially, within the concentration range that exerted effective antiplatelet effects, DHM did not significantly affect any of the tested coagulation parameters, and no cytotoxicity was observed. These in-vitro findings suggest that DHM is a platelet-specific inhibitor, exerting potent antiplatelet effects while not interfering with normal physiological coagulation processes. Therefore, DHM shows potential as an antithrombotic candidate pending in-vivo studies with a potentially low risk of bleeding, providing crucial experimental evidence and a new direction for the development of safer antithrombotic strategies. Plain Language Summary This study explored the antiplatelet effects of dihydromyricetin (DHM) and its impact on blood clotting. Using lab tests, researchers found that DHM effectively reduced platelet activation and aggregation without affecting normal blood clotting or causing cell damage. DHM worked against various platelet activators like ADP, AA, and collagen, and also prevented spontaneous platelet adhesion and aggregation. Importantly, DHM did not alter coagulation parameters, suggesting it targets platelets specifically. These findings indicate DHM could be a promising antithrombotic agent with a low risk of bleeding, paving the way for safer blood clot prevention strategies in future studies. Text is machine generated and may contain inaccuracies. FAQ