Polysaccharide sulfate 916 inhibits neutrophil-endothelial adhesion.
- Author:
Decheng REN
1
;
Meiyu GENG
;
Guanhua DU
;
Juntian ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cell Adhesion; drug effects; Cells, Cultured; Endothelium, Vascular; cytology; Humans; Intercellular Adhesion Molecule-1; analysis; N-Formylmethionine Leucyl-Phenylalanine; pharmacology; Neutrophils; drug effects; physiology; Polysaccharides; pharmacology; Rats; Rats, Wistar; Sulfuric Acids; pharmacology; Tumor Necrosis Factor-alpha; pharmacology; Vascular Cell Adhesion Molecule-1; analysis
- From: Chinese Medical Journal 2002;115(12):1855-1858
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo study the effect of polysaccharide sulfate 916 (PS916) on neutrophil-endothelial cell adhesion.
METHODSCell adhesion was evaluated by testing neutrophil myeloperoxidase activity. Expression of adhesion molecule in human umbilical vein endothelial cell (HUVEC) was measured by ELISA. The neutrophil activation rate induced by N-formyl-methionyl-leucyl-phenylalanine (fMLP) was tested by nitroblue tetrazolium (NBT) reduction.
RESULTSTumor necrosis factor alpha (TNFalpha, 50 - 800 U/ml) increased the adherence of neutrophil to TNFalpha-stimulated HUVEC in a concentration and time dependent manner. PS916 (0.01 - 1.0 mg/ml) dose-dependently inhibited the adherence of neutrophils to TNFalpha-stimulated HUVEC. fMLP increased the activation rate of neutrophils independent of concentration. PS916 also inhibited the adherence of fMLP-activated neutrophils to HUVEC. Moreover, PS916 inhibited adhesion molecule expression in TNFalpha-stimulated HUVEC.
CONCLUSIONSPS916 inhibited neutrophil-endothelial adhesion. The mechanism of its action was partially related to suppressing the expressions of intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1).
