Department of Pharmacology, College of Medicine and Cardiovascular Medical Research Center, Dongguk University, Gyeongju 780-714, Korea.
Cordycepin (3‘-deoxyadenosine) inhibits human platelet aggregation induced by U46619, a TXA2 analogue
Article first published online: 18 FEB 2010
2006 Royal Pharmaceutical Society of Great Britain
Journal of Pharmacy and Pharmacology
Volume 58, Issue 12, pages 1677–1682, December 2006
How to Cite
Cho, H. J., Cho, J. Y., Rhee, M. H., Lim, C. R. and Park, H. J. (2006), Cordycepin (3‘-deoxyadenosine) inhibits human platelet aggregation induced by U46619, a TXA2 analogue. Journal of Pharmacy and Pharmacology, 58: 1677–1682. doi: 10.1211/jpp.58.12.0016
- Issue published online: 18 FEB 2010
- Article first published online: 18 FEB 2010
- June 8, 2006, August 30, 2006
Cordycepin (3′-deoxyadenosine), which comes from Cordyceps militaris, the Chinese medicinal fungal genus Cordyceps, is known to have anti-tumour activity. In this study, we investigated the novel effect of cordycepin on human platelet aggregation that was induced by U46619, a thromboxane A2 (TXA2) analogue. TXA2 is an aggregation-inducing autacoidal molecule that is produced in various agonist-activated platelets. Cordycepin completely inhibited U46619-induced platelet aggregation and simultaneously reduced cytosolic free Ca2+ ([Ca2+]i), which was increased by U46619 (5 μM) up to 66%. Furthermore, the U46619-stimulated phosphorylation of Ca2+-dependent proteins (20 kDa of a myosin light chain and 47 kDa of pleckstrin) was strongly inhibited by cordycepin. These results suggest that cordycepin may have a beneficial effect on autacoidal TXA2-mediated thrombotic diseases by inhibiting TXA2-induced platelet aggregation via suppression of the Ca2+ level.