脂多糖对大鼠小气道上皮细胞TNF-α,TNFR表达和结构的影响

Study on Rat Small Airway Epithelium Injury Induced by Lipopolysac-charide and Its Pathogenesis

探讨脂多糖（LPS）引起大鼠小气道上皮细胞损伤及机制。将SD大鼠随机分为脂多糖气管注射组（LPS100μg /100μl L1组,50μg/100μl L2组）和对照组（生理盐水100μl,C组）。光镜和透射电镜动态观察小气道上皮细胞损伤改变,以原位分子杂交方法检测小气道上皮细胞TNFαmRNA和TNF受体mRNA表达的变化。结果:L1组和L2组病理改变趋势相似。LPS注射2d后,小气道上皮细胞轻度变性;LPS注射4d后,上皮细胞坏死,脱落明显,周围炎症也加重。与C组比较,L1组各时间处死大鼠小气道上皮细胞TNFαmRNA和TNF受体mR-NA表达均增高（P<0.01）;L1组:d8 TNFαmRNA比 d4TNFαmRNA表达明显增强（P<0.05）。L1组d4和d8TNF受体mRNA分别比d2 TNF受体mRNA表达增强（P<0.01）。脂多糖在体内可引起大鼠小气道上皮细胞明显损伤;小气道上皮细胞TNFαmRNA表达上调在脂多糖引起上皮细胞损伤中具有重要作用。

To study rat small airway epithelium injury induced by lipopolysaccharide(LPS) . SD rats were randomly divided into three groups: LPS injection group (group L1, inject 100 fig/100 /ul LPS into rat airway); LPS injection group (group L2, inject 50 ug/100 ul LPS into rat airway) and control group (group C, inject 100 ul physical saline into rat trachea) .Observed dynamically rat small airway epithelium injury changes under LM and TEM. Analysed rat small airway epithelium cell TNFαmRNA and TNF receptor mRNA expression level changes by hybridizationin situ. Results showed that Group L1 and group L2' s pathologic changes were almost same. 2 days after LPS injection small airway epithelium cell were slight degeneration, 4 days after LPS injection, epithelium cells demonstrate obvious necrosis and small airway inflammation also became severe. Group L1 rat small airway epithelium cells TNF am RNA and TNF receptor mRNA were higher(P < 0.01) than that of control group rats. In group L1 ,TNFαmRNA of 8 day were higher than that of 4 days( P < 0.01), and TNF receptor mRNA of 4 days were higher than that of 2 days( P < 0.01) .1. LPS can induce rat small airway epithelium cells obvious injury in vivo. 2. Small airway epithelium cells TNFαmRNA expression increase play a important role in epithelium cell injury induced by LPS.