Antithrombotic Effect of Dioscin in Collagen-induced Human Platelets by Regulation of Cyclic Nucleotides

The discovery and application of new substances that can regulate and reduce platelet activation are important for the prevention and treatment of cardiovascular diseases. Previous studies have shown that dioscin inhibits the growth of tumor-related cells and induces apoptosis. In addition, although there have been a few reports on the antiplatelet effect of dioscin, there has been no study that elucidated the mechanism of platelet activation using human platelets. Therefore, in this study, we confirmed whether dioscin has an antithrombotic effect by regulating the activation of human platelets. Dioscin increased cAMP and cGMP in human platelets, preventing Ca²⁺ mobilization by inducing IP₃R phosphorylation, and inhibited the binding between integrin αIIb/β₃ and fibrinogen by inducing VASP phosphorylation. Finally, dioscin was shown to significantly inhibit thrombin-induced fibrin thrombus formation. Therefore, dioscin has been shown to possess antiplatelet effects that can slow or halt thrombus formation by regulating the phosphorylation of various signaling molecules and related proteins.