【摘要】 探讨了脂多糖 (LPS)诱导大鼠小气道上皮细胞损伤后细胞间黏附分子 (ICAM 1)表达的机制。将SD大鼠随机分为LPS鼻腔注入组 (A组 ) ,LPS气管注入组 (B组 )和正常对照组 (C组 )采用光镜和透射电镜动态观察LPS对小气道上皮细胞损伤改变 ,以免疫组织化学分析方法及原位分子杂交方法检测小气道上皮细胞I CAM 1表达及转录的变化。结果表明A组和B组病理改变相似。存在明显的炎症反应 ,细胞坏死 ,脱落明显。LPS注入后 ,各时间组ICAM 1表达及转录与C组比较 ,均明显增高 (P <0 .0 1) ,A组随LPS注入后d2、d4、d8,ICAM 1mRNA表达逐渐增强 ,与前一时间组相比 (P <0 .0 1)。说明在LPS诱导的大鼠小气道上皮细胞损伤中ICAM 1参与并介导了炎症反应 ,结合上次报道的实验结果证实了小气道上皮细胞黏附分子的表达可受多种细胞因子调控更多还原

【Abstract】 To study rats small airway epithelium injury induced by lipopoly- saccharide(LPS) and its mechanism of ICAM-1 mRNA expression. SD rats were randomly divided into three groups: LPS nasal cavity immit group(group A) LPS trachea injection group (group B) and control group (group C, inject 100()μl physical saline into rats trachea). The small airway epithelium injury changes in rats were observed dunamically. The ICAM-1 mRNA expression level changes were anacy sed by immunohistochemistry and hybridization in situ. Results showed that pathologic changes in grow A were almost the same as in group B. After LPS injection,ICAM-1 mRNA expression level were obvious higher(P<0.01), than that of control. After LPS immit group A ICAM-1 mRNAexpression gradually increaase (P<(0.01)) compared with earlier group. The ICAM-1 pernaps mediate inflammation response in LPS induce rats small airway epithelium cell injury induced my LPS. Combine experiment result in the report last time, Prove ICAM-1 mRNA expression on small airway epithelium cells may controlled by manifold cell factors.更多还原