Study on the mechanism of AHV-PI on platelet aggregation by PI3K/Akt signal pathway
Objective To investigate the mechanism of platelet inhibitor from Agkistrodon halys venom (AHV-PI) on platelet aggregation. Methods Protein kinase Akt phosphorylation levels in platelet were measured by Western blot. XS-1000I blood cell counter was used for platelet count. The plasma content of 5'-NT and platelet membrane GPIb were determined by Enzyme-Linked Immunosorbnent Assay (ELISA). The effect of AHV-PI on binding rate between the fluorescence labeled monoclonal antibody CD61 (FITC-CD61) and platelet membrae glycoprotein Ⅱb/Ⅲa (GPⅡb/Ⅲa) was observed by flow cytometry (FCM). Results AHV-PI can reduce the level of Akt-phosphorylation level and the number of platelet. AHV-PI can increase the content of 5'-NT in plasma, reduce the expression of platelet GPIb. Flow cytometry displayed AHV-PI can not affect the rate of combination between platelet GPⅡb/Ⅲa and FITC-CD61. Conclusion The mechanism of inhibition of platelet aggregation may be inhibit protein kinase Akt phosphorylation to block the signal transduction pathway of Akt. Limit cell grouth and reduce platelet number, also it may be related to its 5'-NT activity, it can degradate ADP to prevent the formation of platelet thrombus.
NETL
NSTL
万方数据
维普
