目的 :观察尼古丁对中性粒细胞 (PMNs)的活化 ,PMNs与内皮细胞的粘附及内皮细胞表达ICAM - 1mRNA ,有助于阐明尼古丁在慢性阻塞性肺疾患 (COPD)炎症发病中的作用。方法 :测定 β -葡萄糖醛酸苷酶及溶菌酶活性 ,以反映PMNs的活化 ;培养人脐静脉内皮细胞 ,观察PMNs与内皮细胞的粘附 ;制备探针 ,提取总RNA ,Northern杂交测细胞间粘附分子 - 1(ICAM - 1)mRNA。结果 :尼古丁可活化PMNs ,增加PMNs-内皮细胞粘附 ;增强ICAM - 1mRNA表达 ,76 4- 3可明显抑制尼古丁的上述作用。结论 :尼古丁通过活化PMNs,促进PMNs -内皮细胞粘附 ,在COPD慢性炎症发病中起重要作用。而这种粘附作用的增加与粘附分子表达增强有关 ;抑制尼古丁的上述作用可能是 76 4- 3抗炎作用的部分机理 AIM: To observe the effects of nicotine on the activation of neutrophils (PMNs), the adhesion of PMNs to endothelial cells and the expression of ICAM - 1 mRNA in endothelial cells, which may help to clarify the role of nicotine in the pathogenesis of chronic obstructive pulmonary disease (COPD). Methods: The activity of β - glucuronidase and lysozyme were measured to reflect the activation of PMNs. The cultured human umbilical vein endothelial cells were cultured and the adhesion of PMNs and endothelial cells was observed. The probes were prepared and the total RNA was extracted. Adhesion molecule - 1 (ICAM - 1) mRNA. Results: Nicotine could activate PMNs, increase PMNs - endothelial cell adhesion and enhance the expression of ICAM - 1 mRNA. 76 4- 3 can obviously inhibit the above effects of nicotine. CONCLUSIONS: Nicotine plays an important role in the pathogenesis of COPD chronic inflammation by activating PMNs and promoting PMNs-endothelial cell adhesion. This increase in adhesion was associated with increased expression of adhesion molecules; the above effect of nicotine inhibition may be part of the mechanism of anti-inflammatory effects of 76-4