Antiplatelet activity of caffeic acid phenethyl ester is mediated through a cyclic GMP-dependent pathway in human platelets

Tyng-Guey Chen, Jie Jen Lee, Kuang Hung Lin, Chia Hung Shen, Duen Suey Chou, Joen Rong Sheu

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The aim of this study was to examine the inhibitory mechanisms of caffeic acid phenethyl ester (CAPE), which is derived from the propolis of honeybee, in platelet activation. In this study, CAPE (15 and 25 μM) markedly inhibited platelet aggregation stimulated by collagen (2 μg/ml). CAPE (15 and 25 μM) increased cyclic GMP level, and cyclic GMP-induced vasodilator-stimulated phosphoprotein (VASP) Ser157 phosphorylation, but did not increase cyclic AMP in washed human platelets. Rapid phosphorylation of a platelet protein of Mw. 47,000 (P47), a marker of protein kinase C activation, was triggered by phorbol-12, 13-dibutyrate (150 nM). This phosphorylation was markedly inhibited by CAPE (15 and 25 μM). The present study reports a novel and potent antiplatelet agent, CAPE, which involved in the following inhibitory pathways: CAPE increases cyclic GMP/VASP Ser157 phosphorylation, and subsequently inhibits protein kinase C activity, resulting in inhibition of P47 phosphorylation, which ultimately inhibits platelet aggregation. These results strongly indicate that CAPE appears to represent a novel and potent antiplatelet agent for treatment of arterial thromboembolism.

Original languageEnglish
Pages (from-to)121-126
Number of pages6
JournalChinese Journal of Physiology
Issue number3
Publication statusPublished - 2007



  • Caffeic acid phenethyl ester
  • Cyclic GMP
  • Protein kinase C
  • Vasodilator-stimulated phosphoprotein

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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