Activation of platelet-neutrophil mediated by platelet-activating factor.
- Author:
Nong-Jian GUO
1
;
Ya-Li CHANG
;
Dong-Jie XIAO
;
Ping HUANG
Author Information
1. Department of Hematology, Ji'nan Central Hospital, Clinical Medical College, Shandong University, Ji' nan 250013, China. gujian2002@yahoo.com.cn
- Publication Type:Journal Article
- MeSH:
Adenosine Diphosphate;
pharmacology;
Adult;
Blood Platelets;
cytology;
drug effects;
physiology;
CD11b Antigen;
blood;
Cell Adhesion;
drug effects;
physiology;
Cell Communication;
drug effects;
physiology;
Female;
Flow Cytometry;
Ginkgolides;
pharmacology;
Humans;
Male;
Middle Aged;
Neutrophils;
cytology;
drug effects;
physiology;
P-Selectin;
blood;
Platelet Activating Factor;
pharmacology;
Platelet Activation;
drug effects;
Platelet Glycoprotein GPIb-IX Complex;
analysis;
Platelet Membrane Glycoproteins;
antagonists & inhibitors;
physiology;
Receptors, G-Protein-Coupled;
antagonists & inhibitors;
physiology
- From:
Journal of Experimental Hematology
2005;13(3):447-451
- CountryChina
- Language:Chinese
-
Abstract:
To investigate the pathophysiological mechanisms for platelet-neutrophils cross talk mediated by platelet-activating factor (PAF) and to lay a foundation for clinical application, ginkgolides B (GB), a PAF receptor antagonist, was added in the whole blood to block the effects of PAF on activation of platelet-neutrophil; PAF and ADP were respectively added in the whole blood to monitor the expression of CD62P on platelet by flow cytometry; PAF and ADP were added in the whole blood to monitor the expression of CD11b on neutrophil by flow cytometry; PAF and ADP were added in the whole blood to monitor the platelet-leucocyte aggregates (PLA) which were PLA in the total leucocyte population (PLA/L) and the mean fluorescence intensity (MFI) of CD42b. Outcomes were analyzed by t-test, and the differences were statistically significant (P < 0.05). The results showed that the expression of CD62P on platelats, the expression of CD11b on neutrophils and PLA formation were all increased by PAF and ADP; the PAF receptor antagonists (GB) could obviously inhibit the expression of CD62P, CD11b and PLA formation induced by PAF, but could not completely inhibit the activation of platelet and neutrophil, and the platelet-neutrophil cross talk; GB could inhibit the expression of CD62P and CD11b induced by ADP, but could not conpletely inhibit the activation of platelet and neutrophli; GB could not obviously inhibit the platelet-leucocyte aggregates mediated by ADP. It is concluded that the multiligand-receptor systems involved in PLA formation and platelet-netrophils cross talk seem to be regulated by complex mechanisms; the PAF receptor antagonists (GB) obviously inhibit the effect of PAF, and may be widely utilized in the therapy of thrombosis and inflammation.
