Salidroside inhibits platelet function and thrombus formation through AKT/GSK3β signaling pathway
Guangyu Wei, Xiao‐Qi Xu, Huan Tong, Xiamin Wang, Yuting Chen, Yangyang Ding, Sixuan Zhang, Wen Ju, Chunling Fu, Zhenyu Li, Lingyu Zeng, Kailin Xu, Jianlin Qiao
Abstract
. 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.