Antiplatelet Effects of Hydroxygenkwanin via the Regulation of Cyclic Nucleotides and Ca²⁺ Mobilization on Collagen-Induced Human Platelets

Cardiovascular disease (CVD) is a major cause of death and is treated using various antiplatelet agents. Recently, several efforts have been made to develop antiplatelet agents from natural biologically active compounds due to the side effects of the antiplatelet agent currently used. Hydroxygenkwanin is a major component of Daphne genkwa and has been reported to prevent thrombosis by inhibiting tissue factors and to have antibacterial, anti-inflammatory, and anticancer effects. However, little is known about its antiplatelet effect or mode of action. This study confirms the effect of hydroxygenkwanin on collagen-induced human platelets and reports that hydroxygenkwanin induces the phosphorylations of VASP and IP3R by increasing the productions of cAMP and cGMP and activating dependent kinases and thus inhibiting the translocation of Ca 2+ to cytoplasm, fibrinogen binding, and fibrin clot formation. Our findings suggest that hydroxygenkwanin has potential for the treatment of CVD by inhibiting platelet activation and thrombus formation.