Anti-platelet activity of panaxatriol saponins is mediated by suppression of intracellular calcium mobilization and ERK2/p38 activation

被引：33

作者：

Qi, Hongyi ^{[1
]}

Huang, Yongliang ^{[2
]}

Yang, Yi ^{[1
]}

Dou, Guojun ^{[1
]}

Wan, Fang ^{[3
]}

Zhang, Wenwu ^{[3
]}

Yang, Huarong ^{[3
]}

Wang, Li ^{[3
]}

Wu, Chunjie ^{[4
]}

Li, Li ^{[1
]}

机构：

[1] Southwest Univ, Coll Pharmaceut Sci, 2 Tiansheng Rd, Chongqing 400716, Peoples R China

[2] Chengdu Univ Tradit Chinese Med, Affiliated Hosp, Chengdu 610075, Sichuan, Peoples R China

[3] Huasun Grp Co Ltd, Chengdu 610072, Sichuan, Peoples R China

[4] Chengdu Univ Tradit Chinese Med, Coll Pharm, Chengdu 611137, Sichuan, Peoples R China

来源：

BMC COMPLEMENTARY AND ALTERNATIVE MEDICINE | 2016年 / 16卷

关键词：

Panaxatriol saponin; Platelet aggregation; Intracellular calcium mobilization; p-ERK2; p-p38; PLATELET-AGGREGATION; THROMBUS FORMATION; GLYCOPROTEIN-VI; INVOLVEMENT; ROLES; P38; RECEPTORS; ADHESION;

D O I：

10.1186/s12906-016-1160-7

中图分类号：

R [医药、卫生];

学科分类号：

10 ;

摘要：

Background: Increased platelet aggregation is implicated in the pathogenesis of ischemic stroke and anti-platelet strategy may contribute to its therapy. Panaxatriol saponin (PTS), the main components extracted from Panax notoginseng, has been shown to be efficacious in the prevention and treatment of ischemic stroke in China. The aim of this study is to determine the anti-platelet activity and explore the underlying mechanisms. Methods: Inhibitory effect of PTS and its main ginsenosides on agonists-induced platelet aggregation was determined using rabbit or human platelets. Intracellular Ca2+ concentration ([Ca2+]i) mobilization was detected with fura-2/AM probe. MAPKs phosphorylation was determined by Western blotting. Results: Our results showed PTS inhibited the rabbit platelet aggregation induced by various agonists (collagen, thrombin and ADP). The three main ginsenosides (Rg1, Re and R1) existing in PTS also showed anti-platelet activity, while their combination exhibited no synergistic effect on rabbit platelet aggregation. Further study demonstrated that PTS and its main ginsenosides also exhibited inhibitory effect on human platelet aggregation. Mechanism study demonstrated that pre-treatment with PTS inhibited the agonists-induced intracellular calcium mobilization. Moreover, PTS significantly suppressed the activation of both ERK2 and p38 by the agonists via reducing the phosphorylation of ERK2 and p38. Conclusion: We proved that PTS is effective in anti-platelet aggregation, which may, at least in part, be related to the suppression of intracellular calcium mobilization and ERK2/p38 activation. This study may provide one reasonable explanation for the efficacy of PTS on the prevention and treatment of ischemic stroke.

引用

页数：8