Key result
Ginkgo biloba extract reduces platelet adhesion and activation by attenuating the PI3K/Akt pathway.
Ginkgo biloba extract inhibits platelet activation and aggregation, a process that appears to be mediated by the attenuation of the PI3K/Akt pathway.
Animal data on Ginkgo biloba's platelet effects are hypothesis-generating; human trials required before any clinical consideration.
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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Ye et al. (2015) studied this question. Ginkgo biloba extract (GBE) was evaluated on Platelet aggregation, adhesion, and Akt phosphorylation. Ginkgo biloba extract reduced platelet adhesion and spreading, and inhibited Akt phosphorylation, suggesting its anti-platelet activation effects are mediated by attenuating the PI3K/Akt pathway.
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