Bactericidal permeability increasing protein inhibits lipopolysaccharide-mediated platelet activation in vitro / 中国实验血液学杂志
Journal of Experimental Hematology
;
(6): 129-132, 2012.
Article
in Chinese
| WPRIM
| ID: wpr-331005
ABSTRACT
This study was purposed to investigate the inhibitory effect of bactericidal permeability-increasing protein (BPI) on lipopolysaccharide (LPS)-mediated activation of platelets. Venous blood samples were obtained from 10 healthy volunteers and were prepared into platelet-rich plasma (PRP, 1 × 10(8)/ml). Experiments were divided into four groups normal platelet group (untreated group); LPS group, BPI group and BPI+LPS group. PRP were stimulated by LPS (10 µg/ml) in the presence and absence of BPI (100 µg/ml) or BPI alone. Then platelets were harvested and determined for Toll-like receptor-4 (TLR-4) with flow cytometry (FCM), the supernatant was used for detection of cytokines including tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) with enzyme-linked immunosorbent assay (ELISA). The results showed that as compared with normal platelet group, TLR-4 expression on platelets was significantly increased under LPS stimulation (P < 0.001); the levels of TNF-α and IL-6 in the supernatant were also remarkably elevated (P < 0.001). However, either TLR-4 expression or the cytokine levels significantly decreased in the presence of BPI when platelets underwent LPS-challenge (P < 0.05), but still were higher than that in normal platelet group. Stimulating the platelets with BPI alone could not enhance the TLR-4 expression and cytokine levels. It is concluded that BPI has the ability to inhibit the LPS-induced platelet activation.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Pharmacology
/
Blood Proteins
/
Platelet Activation
/
Lipopolysaccharides
/
Antimicrobial Cationic Peptides
/
Toll-Like Receptor 4
/
Platelet-Rich Plasma
/
Inflammation
/
Metabolism
Limits:
Humans
Language:
Chinese
Journal:
Journal of Experimental Hematology
Year:
2012
Type:
Article
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