Vasodilator-stimulated phosphoprotein-phosphorylation by ginsenoside Ro inhibits fibrinogen binding to αIIb/β₃ in thrombin-induced human platelets

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• 作者：Jung-Hae Shin¹ ; ^☆ ; Hyuk-Woo Kwon¹ ; ^☆ ; Hyun-Jeong Cho² ; Man Hee Rhee³ ; Hwa-Jin Park¹ ; ^{mlsjpark@inje.ac.kr" class="auth_mail" title="E-mail the corresponding author}
• 关键词：cAMP ; clot retraction ; ginsenoside Ro ; fibrinogen binding ; VASP (Ser157)
• 刊名：Journal of Ginseng Research
• 出版年：2016
• 出版时间：October 2016
• 年：2016
• 卷：40
• 期：4
• 页码：359-365
• 全文大小：1124 K

文摘

Glycoprotein IIb/IIIa (αIIb/β₃) is involved in platelet adhesion, and triggers a series of intracellular signaling cascades, leading to platelet shape change, granule secretion, and clot retraction. In this study, we evaluated the effect of ginsenoside Ro (G-Ro) on the binding of fibrinogen to αIIb/β₃.

Methods

We investigated the effect of G-Ro on regulation of signaling molecules affecting the binding of fibrinogen to αIIb/β₃, and its final reaction, clot retraction.

Results

We found that G-Ro dose-dependently inhibited thrombin-induced platelet aggregation and attenuated the binding of fibrinogen to αIIb/β₃ by phosphorylating cyclic adenosine monophosphate (cAMP)-dependently vasodilator-stimulated phosphoprotein (VASP; Ser¹⁵⁷). In addition, G-Ro strongly abrogated the clot retraction reflecting the intensification of thrombus.

Conclusion

We demonstrate that G-Ro is a beneficial novel compound inhibiting αIIb/β₃-mediated fibrinogen binding, and may prevent platelet aggregation-mediated thrombotic disease.