摘要目的研究硫酸多糖916对中性粒细胞-内皮细胞粘附的作用. 方法通过检测中性粒细胞髓过氧化酶的活性观察细胞(HUVEC)粘附作用.用ELISA法测定人脐静脉内皮细胞粘附分子.用硝基蓝四唑(NBT)还原法测定N-甲酰甲硫亮氨酰苯丙氨酸(fMLP)对中性粒细胞的激活率. 结果 TNFα (50-800 U/ml)以剂量和时间依赖性的方式增强中性粒细胞对TNFα刺激的HUVEC的粘附作用.硫酸多糖916 (0.01-1.0 mg/ml)剂量依赖性地抑制二者的粘附.fMLP增加中性粒细胞的激活,且呈剂量依赖性.硫酸多糖916抑制fMLP活化的中性粒细胞对HUVEC的粘附作用,而且抑制TNFα刺激的HUVEC粘附分子的表达.结论硫酸多糖916具有抑制中性粒细胞-内皮细胞粘附的作用,作用机制与抑制内皮细胞附分子ICAM-1和VCAM-1的表达有关.

abstractsObjective 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 (TNFα, 50-800 U/ml) increased the adherence of neutrophil to TNFα-stimulated HUVEC in a concentration and time dependent manner. PS916 (0.01-1.0 mg/ml) dose-dependently inhibited the adherence of neutrophils to TNFα-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 TNFα-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).