Antiplatelet effect of butylidenephthalide

• DOI: 10.1016/0304-4165(87)90151-6
• Publication Date: 2003-02-11T02:49:56Z
• Authors: Che-Ming Teng; Wen-Ying Chen; Wun-Chang Ko; Chaoho Ouyang
• Keywords: 0301 basic medicine; Arachidonic Acid; Platelet Aggregation; Prostaglandins E; Guinea Pigs; Phthalic Acids; Thrombin; Arachidonic Acids; In Vitro Techniques; Blood Coagulation Factors; Dinoprostone; 3. Good health; Adenosine Diphosphate; Thromboxane B2; 03 medical and health sciences; Adenosine Triphosphate; Phthalic Anhydrides; Animals; Humans; Collagen; Rabbits; Platelet Activating Factor; Calcimycin

Butylidenephthalide inhibited, in a dose-dependent manner, the aggregation and release reaction of washed rabbit platelets induced by collagen and arachidonic acid. Butylidenephthalide also inhibited slightly the platelet aggregation induced by PAF and ADP, but not that by thrombin or ionophore A23187. Thromboxane B2 formation caused by collagen, arachidonic acid, thrombin and ionophore A23187 was in each case markedly inhibited by butylidenephthalide. Butylidenephthalide inhibited the aggregation of ADP-refractory platelets, thrombin-degranulated platelets, chymotrypsin-treated platelets and platelets in the presence of creatine phosphate/creatine phosphokinase. Its inhibition of collagen-induced aggregation was more marked at lower Ca2+ concentrations in the medium. The aggregability of platelets inhibited by butylidenephthalide could be recovered after the washing of platelets. In human platelet-rich plasma, butylidenephthalide and indomethacin prevented the secondary aggregation and blocked ATP release from platelets induced by epinephrine. Prostaglandin E2 formed by the incubation of guinea-pig lung homogenate with arachidonic acid could be inhibited by butylidenephthalide, indomethacin and aspirin. It is concluded that the antiplatelet effect of butylidenephthalide is mainly due to an inhibitory effect on cyclo-oxygenase and may be due partly to interference with calcium mobilization.