Inhibitory effects of atractylenolide 3 on platelet and its mechanism
10.13220/j.cnki.jipr.2016.03.021
- Author:
Yi-Zhu CHEN
1
Author Information
1. Department of Cardiology, No.9 People’s Hospital Affiliated to Shanghai Jiao Tong University, School of Medicine
- Publication Type:Journal Article
- Keywords:
Atractylenolide 3;
Cardiovascular disease;
Platelet;
Thrombus
- From:
Journal of International Pharmaceutical Research
2016;43(3):514-517
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the effects of atractylenolide 3 on human platelet in vitro and explore the underlying mechanism. Methods The effects of atractylenolide 3 on human platelet aggregation induced by thrombus alkane analogues (U46619) was tested by turbidimetry in vitro. ATP secretion weas detected by luciferase detection, and the phosphorylation levels of Erk and Akt were detected by Western blotting. Results Atractylenolide 3 diminished U46619-induced human platelet aggregation in concentration dependence. Compared with DMSO control group, the inhibitory rate were significant increased in each experiment group (P<0.01). Atractylenolide 3 inhibited adenosine triphosphate (ATP) secreted by human platclet in concentration dependence. Compared with the DMSO control group, the inhibitory rate were significant increased in each experiment group (P<0.01), and the levels of phospho- Akt (Ser473) and phospho- Erk1/2 were significant downregulated in the presence of atractylenolide 3 in each experiment group (P<0.01). Conclusion Atractylenolide 3 exhibits a concentration-dependent inhibitory effect on human platelet aggregation and secretion induced by U46619. Also, it regulated the MAPK and PI3K-Akt signaling pathways. These results show that atractylenolide 3 is an effective antiplatelet compound, may serve as new antithrombotic drugs.
