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Inhibitory Effects of Scopoletin in Collagen-induced Human Platelet Aggregation
Korean J Clin Lab Sci 2019;51:34-41  
Published on March 31, 2019
Copyright © 2019 Korean Society for Clinical Laboratory Science.

Hyuk-Woo Kwon1, Jung-Hae Shin1, Chang-Eun Park2, Dong-Ha Lee2

1Department of Biomedical Laboratory Science, Far East University, Eumseong, Korea, 2Department of Biomedical Laboratory Science, Molecular Diagnostics Research Institute, Namseoul University, Cheonan, Korea
Correspondence to: Dong-Ha Lee
Department of Biomedical Laboratory Science, Molecular Diagnostics Research Institute, Namseoul University, 91 Daehak-ro, Seonghwan-eup, Seobuk-gu, Cheonan 31020, Korea, Tel: 82-41-580-2148, Fax: 82-41-580-2932, E-mail:, ORCID:
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Platelet aggregation is essential for the formation of a hemostatic plug in the case of blood vessel damage. On the other hand, excessive platelet aggregation may cause cardiovascular disorders, such as thrombosis, atherosclerosis, and myocardial infarction. Scopoletin, which found in the root of plants in the genus Scopolia or Artemisia, has anti-coagulation and anti-malaria effects. This study examined the effects of scopoletin on human platelet aggregation induced by collagen. Scopoletin had anti-platelet effects via the down-regulation of thromboxane A2 (TXA2) production and intracellular Ca2+ mobilization ([Ca2+]i), which are aggregation-inducing molecules produced in activated platelets. On the other hand, scopoletin increased both the cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) levels, which are known as intracellular Ca2+-antagonists and aggregation-inhibiting molecules. In particular, scopoletin increased the potently cAMP level more than cGMP, which led to suppressed fibrinogen binding to αIIb/β3 in collagen-induced human platelet aggregation. In addition, scopoletin inhibited collagen-elevated adenosine triphosphate (ATP) release in a dose-dependent manner. The results suggest that aggregation amplification through granule secretion is inhibited by scopoletin. Therefore, scopoletin has potent anti-platelet effects and may have potential for the prevention of platelet-derived vascular diseases.
Keywords : Cyclic nucleotide, Intracellular Ca2+, Scopoletin, Thromboxane A2

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