Ginkgo biloba Extract Inhibits Platelet Activation via Inhibition of Akt

Shiyong Ye, Xiang Yijia, Zhong Peng, Liu Chong, Wuming Hu, Linchun Lv, Zeng Chunlai
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引用次数: 6

Abstract

Ginkgo biloba extract (GBE) contains flavone glycosides and terpenoids. It can modify vasomotor function, reduce the adhesion of blood cells to the endothelium, and inhibit the activation of platelets, and therefore plays an important role in the treatment of a variety of cardiovascular and neurological disorders. However, the molecular mechanism underlying its significant anticoagulation activity is largely unknown. In this study, we found that GBE adenosine diphosphate, collagen, and U4 (U46619) induced platelet aggregation in both platelet-rich plasma and washed platelets. GBE could reduce the adhesion of platelets to a collagen-coated surface and platelet spreading on fibrinogen. The treatment with GBE significantly inhibited the phosphorylation of Akt, suggesting that its inhibition of platelet activation might be mediated by attenuation of the PI3K/Akt pathway.
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银杏叶提取物通过抑制Akt抑制血小板活化
银杏叶提取物(GBE)含有黄酮类苷和萜类化合物。它可以改变血管舒缩功能,减少血细胞对内皮的粘附,抑制血小板的活化,因此在治疗多种心血管和神经系统疾病中起重要作用。然而,其显著抗凝活性的分子机制在很大程度上是未知的。在这项研究中,我们发现GBE二磷酸腺苷、胶原蛋白和U4 (U46619)在富血小板血浆和洗涤血小板中诱导血小板聚集。GBE可以降低血小板对胶原包被表面的粘附和血小板在纤维蛋白原上的扩散。GBE显著抑制Akt的磷酸化,提示其对血小板活化的抑制可能是通过抑制PI3K/Akt通路介导的。
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