EFFECT OF ASPIRIN ON TNFα INDUCED ADHESION OF ENDOTHELIAL-NEUTROPHIL AND ENDOTHELIAL-MONOCYTE

AIM　To study the effect of aspirin on TNFα induced adhesion of endothelial-neutrophil and endothelial-monocyte and its mechanism. METHODS　Cell adhesion was measured by testing leukocyte myeloperoxidase activity; expression of adhesion molecules was measured by ELISA. RESULTS　Aspirin（600 mg.L^-1, 900 mg.L^-1） was shown to inhibit endothelial cells(EC) which were stimulated by TNF_α for 6 h binding to neutrophil and monocyte. The rate of inhibition for endothelial-neutrophil adhesion was 13.4% and 23.2% respectively; and that for endothelial-monocyte adhesion was 14.9% and 24.3% respectively. If the time of stimulation was extended to 24 h, the effect of aspirin on endothelial-monocyte adhesion was more potent(rate of inhibition： 20.0% and 38.9%), while it showed no effect on endothelial-neutrophlil adhesion. This discrepancy was due to the selective inhibition of aspirin on adhesion molecules. CONCLUSION　Aspirin inhibited TNF_α-stimulated endothelial-neutrophil adhesion by suppressing the expressions of E-selectin while inhibited endothelial-monocyte adhesion by suppressing the expression of VCAM-1.