Research Paper Volume 12, Issue 9 pp 8151—8166

Salidroside inhibits platelet function and thrombus formation through AKT/GSK3β signaling pathway

Guangyu Wei1,2,3, *, , Xiaoqi Xu1,2,3, *, , Huan Tong1,2,3, *, , Xiamin Wang1,2,3, , Yuting Chen1,2,3, , Yangyang Ding1,2,3, , Sixuan Zhang1,2,3, , Wen Ju1,2,3, , Chunling Fu1,2,3, , Zhenyu Li1,2,3, , Lingyu Zeng1,2,3, , Kailin Xu1,2,3, , Jianlin Qiao1,2,3, ,

  • 1 Blood Diseases Institute, Xuzhou Medical University, Xuzhou, China
  • 2 Department of Hematology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, China
  • 3 Key Laboratory of Bone Marrow Stem Cell, Xuzhou, China
* Equal contribution

Received: December 17, 2019       Accepted: March 30, 2020       Published: April 30, 2020
How to Cite

Copyright © 2020 Wei et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Salidroside is the main bioactive component in Rhodiola rosea and possesses multiple biological and pharmacological properties. However, whether salidroside affects platelet function remains unclear. Our study aims to investigate salidroside’s effect on platelet function. Human or mouse platelets were treated with salidroside (0-20 μM) for 1 hour at 37°C. Platelet aggregation, granule secretion, and receptors expression were measured together with detection of platelet spreading and clot retraction. In addition, salidroside (20 mg/kg) was intraperitoneally injected into mice followed by measuring tail bleeding time, arterial and venous thrombosis. Salidroside inhibited thrombin- or CRP-induced platelet aggregation and ATP release and did not affect the expression of P-selectin, glycoprotein (GP) Ibα, GPVI and αIIbβ3. Salidroside-treated platelets presented decreased spreading on fibrinogen or collagen and reduced clot retraction with decreased phosphorylation of c-Src, Syk and PLCγ2. Additionally, salidroside significantly impaired hemostasis, arterial and venous thrombus formation in mice. Moreover, in thrombin-stimulated platelets, salidroside inhibited phosphorylation of AKT (T308/S473) and GSK3β (Ser9). Further, addition of GSK3β inhibitor reversed the inhibitory effect of salidroside on platelet aggregation and clot retraction. In conclusion, salidroside inhibits platelet function and thrombosis via AKT/GSK3β signaling, suggesting that salidroside may be a novel therapeutic drug for treating thrombotic or cardiovascular diseases.


CRP: collagen-related peptide; GP: glycoprotein; Syk: spleen tyrosine kinase; PLCγ2: phospholipase Cγ2; ACD: acid citrate dextrose; DVT: deep vein thrombosis; IVC: inferior vena cava; GSK-3β: glycogen synthase kinase-3β.