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目的 :研究细菌脂多糖 (LPS)诱导的肺微血管内皮细胞 (PMVEC)与多形核中性粒细胞 (PMN)的粘附作用及调控机制 ;方法 :1 0 0ng/mlLPS刺激PMVEC 0h、2h、4h、6h、8h或 1 0ng/ml、50ng/ml、1 0 0ng/mlLPS刺激 6h ,检测PMVEC -PMN粘附率、PMVEC细胞间粘附分子 -1 (ICAM -1 )的表达 ;凝胶电泳迁移率变化分析 (EMSA)方法检测核因子κB(NF -κB)的活化 ,并通过加入Anti ICAM 1抗体或活化阻断剂观察对PMVEC -PMN粘附率的影响 ;结果 :PMVECICAM -1的表达及与PMN的粘附与LPS的刺激呈时相 -剂量依赖方式 ,LPS的刺激迅速活化NF -κB ,60min达到高峰 ,后逐渐下降 ,Anti-ICAM -1抗体、PDTC能显著降低PMVEC -PMN粘附 (P <0 .0 0 1 ) ;结论 :LPS刺激诱导NF -κB的活化 ,启动ICAM -1的合成表达 ,从而导致PMVEC -PMN的粘附增加。
Objective: To investigate the adhesion and regulation mechanism of pulmonary microvascular endothelial cells (PMV) induced by bacterial lipopolysaccharide (LPS) and polymorphonuclear neutrophils (PMN) .Methods: PMVEC was stimulated with LPS for 0h, 2h, The adhesion rate of PMVEC-PMN and the expression of intercellular adhesion molecule-1 (ICAM-1) in PMVEC were detected by flow cytometry, 4h, 6h, 8h or 10ng / ml, 50ng / ml and 100ng / EMSA was used to detect the activation of nuclear factor kappa B (NF-κB), and the effect of PMVEC-PMN adhesion was observed by adding Anti ICAM 1 antibody or activating blocker.Results: The expression of PMVECICAM -1 And PMN adhesion and LPS stimulation in a time-dose-dependent manner, LPS stimulated the rapid activation of NF-κB, 60min peaked and then decreased, Anti-ICAM -1 antibody, PDTC can significantly reduce PMVEC-PMN stick (P <0.001). CONCLUSION: LPS stimulation induces NF-κB activation and initiates ICAM-1 synthesis, resulting in increased PMVEC-PMN adhesion.