Cordycepin (3‘-deoxyadenosine) inhibits human platelet aggregation induced by U46619, a TXA2 analogue

Authors

  • Hyun Jeong Cho,

    1. Department of Biomedical Laboratory Science, College of Biomedical Science and Engineering, and Regional Research Center, Inje University, 607, Obang-dong, Gimhae, Gyungnam 621-749, Korea.
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    • 4

      Department of Pharmacology, College of Medicine and Cardiovascular Medical Research Center, Dongguk University, Gyeongju 780-714, Korea.

  • Jae Youl Cho,

    1. School of Bioscience and Biotechnology, Kangwon National University, Chuncheon 200-701, Korea.
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  • Man Hee Rhee,

    1. College of Veterinary Medicine, Kyungpook National University, Daegu 702-701, Korea.
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  • Chang Ryul Lim,

    1. Department of Biomedical Laboratory Science, College of Biomedical Science and Engineering, and Regional Research Center, Inje University, 607, Obang-dong, Gimhae, Gyungnam 621-749, Korea.
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  • Hwa Jin Park

    Corresponding author
    1. Department of Biomedical Laboratory Science, College of Biomedical Science and Engineering, and Regional Research Center, Inje University, 607, Obang-dong, Gimhae, Gyungnam 621-749, Korea.
      Department of Biomedical Laboratory Science, College of Biomedical Science and Engineering, Inje University, 607, Obang-dong, Gimhae, Gyungnam 621-749, Korea. E-mail: mlsjpark@inje.ac.kr
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Department of Biomedical Laboratory Science, College of Biomedical Science and Engineering, Inje University, 607, Obang-dong, Gimhae, Gyungnam 621-749, Korea. E-mail: mlsjpark@inje.ac.kr

Abstract

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.

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