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Ginsenoside Rg3-enriched red ginseng extract inhibits platelet activation and in vivo thrombus formationopen access

Authors
Jeong, DahyeIrfan, MuhammadKim, Sung-DaeKim, SukOh, Jun-HwanPark, Chae-KyuKim, Hyun-KyoungRhee, Man Hee
Issue Date
Oct-2017
Publisher
KOREAN SOC GINSENG
Keywords
collagen; ginsenoside Rg3-RGE; Panax ginseng; platelet aggregation
Citation
JOURNAL OF GINSENG RESEARCH, v.41, no.4, pp 548 - 555
Pages
8
Indexed
SCIE
SCOPUS
KCI
Journal Title
JOURNAL OF GINSENG RESEARCH
Volume
41
Number
4
Start Page
548
End Page
555
URI
https://scholarworks.gnu.ac.kr/handle/sw.gnu/13428
DOI
10.1016/j.jgr.2016.11.003
ISSN
1226-8453
2093-4947
Abstract
Background: Korean Red Ginseng has been used for several decades to treat many diseases, enhancing both immunity and physical strength. Previous studies have documented the therapeutic effects of ginseng, including its anticancer, antiaging, and anti-inflammatory activities. These activities are mediated by ginsenosides present in the ginseng plant. Ginsenoside Rg3, an effective compound from red ginseng, has been shown to have antiplatelet activity in addition to its anticancer and anti-inflammatory activities. Platelets are important for both primary hemostasis and the repair of the vessels after injury; however, they also play a crucial role in the development of acute coronary diseases. We prepared ginsenoside Rg3-enriched red ginseng extract (Rg3-RGE) to examine its role in platelet physiology. Methods: To examine the effect of Rg3-RGE on platelet activation in vitro, platelet aggregation, granule secretion, intracellular calcium ([Ca2+] i) mobilization, flow cytometry, and immunoblot analysis were carried out using rat platelets. To examine the effect of Rg3-RGE on platelet activation in vivo, a collagen plus epinephrine-induced acute pulmonary thromboembolism mouse model was used. Results: We found that Rg3-RGE significantly inhibited collagen-induced platelet aggregation and [Ca2+] i mobilization in a dose-dependent manner in addition to reducing ATP release from collagen-stimulated platelets. Furthermore, using immunoblot analysis, we found that Rg3-RGE markedly suppressed mitogen-activated protein kinase phosphorylation (i.e., extracellular stimuli-responsive kinase, Jun Nterminal kinase, p38) as well as the PI3K (phosphatidylinositol 3 kinase)/Akt pathway. Moreover, Rg3RGE effectively reduced collagen plus epinephrine-induced mortality in mice. Conclusion: These data suggest that ginsenoside Rg3-RGE could be potentially be used as an antiplatelet therapeutic agent against platelet-mediated cardiovascular disorders. (C) 2017 The Korean Society of Ginseng, Published by Elsevier Korea LLC.
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