The inhibitory mechanism of crude saponin fraction from korean red ginseng in collagen-induced platelet aggregationopen access
- Authors
- Jeon B.R.[Jeon B.R.]; Kim S.J.[Kim S.J.]; Hong S.B.[Hong S.B.]; Park H.-J.[Park H.-J.]; Cho J.Y.[Cho J.Y.]; Rhee M.H.[Rhee M.H.]
- Issue Date
- Jul-2015
- Publisher
- 고려인삼학회
- Keywords
- crude saponin fraction; Korean Red Ginseng; mitogen-activated protein kinase; phosphatidylinositol-3-kinase; platelet aggregation
- Citation
- Journal of Ginseng Research, v.39, no.3, pp.279 - 285
- Indexed
- SCIE
SCOPUS
KCI
- Journal Title
- Journal of Ginseng Research
- Volume
- 39
- Number
- 3
- Start Page
- 279
- End Page
- 285
- URI
- https://scholarworks.bwise.kr/skku/handle/2021.sw.skku/43407
- DOI
- 10.1016/j.jgr.2015.02.001
- ISSN
- 1226-8453
- Abstract
- Background: Korean Red Ginseng has been used as a traditional oriental medicine to treat illness and to promote health for several thousand years in Eastern Asia. It is widely accepted that ginseng saponins, ginsenosides, are the major active ingredients responsible for Korean Red Ginseng’s therapeutic activity against many kinds of illness. Although the crude saponin fraction (CSF) displayed antiplatelet activity, the molecular mechanism of its action remains to be elucidated. Methods: The platelet aggregation was induced by collagen, the ligand of integrin α<inf>II</inf> β<inf>I</inf> and glycoprotein VI. The crude saponin’s effects on granule secretion [e.g., calcium ion mobilization and adenosine triphosphate (ATP) release] were determined. The activation of mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated protein kinase 1/2 (ERK1/2), c-Jun N-terminal kinases (JNKs), and p38 MAPK, and phosphoinositide 3-kinase (PI3K)/Akt was analyzed by immunoblotting. In addition, the activation of integrin α<inf>II</inf> bβ<inf>III</inf> was examined by fluorocytometry. Results: CSF strongly inhibited collagen-induced platelet aggregation and ATP release in a concentrationdependent manner. It also markedly suppressed [Ca2þ]<inf>i</inf> mobilization in collagen-stimulated platelets. Immunoblotting assay revealed that CSF significantly suppressed ERK1/2, p38, JNK, PI3K, Akt, and mitogen-activated protein kinase kinase 1/2 phosphorylation. In addition, our fraction strongly inhibited the fibrinogen binding to integrin α<inf>IIβ</inf>b<inf>3</inf>. Conclusion: Our present data suggest that CSF may have a strong antiplatelet property and it can be considered as a candidate with therapeutic potential for the treatment of cardiovascular disorders involving abnormal platelet function. © 2015, The Korean Society of Ginseng, Published by Elsevier. All rights reserved.
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Collections - Biotechnology and Bioengineering > Integrative Biotechnology > 1. Journal Articles
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