Shiyong Ye, Xiang Yijia, Zhong Peng, Liu Chong, Wuming Hu, Linchun Lv, Zeng Chunlai
{"title":"Ginkgo biloba Extract Inhibits Platelet Activation via Inhibition of Akt","authors":"Shiyong Ye, Xiang Yijia, Zhong Peng, Liu Chong, Wuming Hu, Linchun Lv, Zeng Chunlai","doi":"10.1159/000381744","DOIUrl":null,"url":null,"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.","PeriodicalId":91502,"journal":{"name":"Integrative medicine international","volume":"380 1","pages":"234 - 242"},"PeriodicalIF":0.0000,"publicationDate":"2015-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000381744","citationCount":"6","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Integrative medicine international","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1159/000381744","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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.