OBJECTIVE: To study the effect of polysaccharide sulfate 916 (PS916) on neutrophil-endothelial cell adhesion. METHODS: Cell adhesion was evaluated by testing neutrophil myeloperoxidase activity. Expression of adhesion...OBJECTIVE: To study the effect of polysaccharide sulfate 916 (PS916) on neutrophil-endothelial cell adhesion. METHODS: Cell 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. RESULTS: Tumor 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. CONCLUSIONS: PS916 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).展开更多
基金ThisworkwassupportedbytheNationalNaturalScienceFoundationofChina (No 30 0 1161940 )
文摘OBJECTIVE: To study the effect of polysaccharide sulfate 916 (PS916) on neutrophil-endothelial cell adhesion. METHODS: Cell 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. RESULTS: Tumor 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. CONCLUSIONS: PS916 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).