东南大学学报（医学版）
東南大學學報（醫學版）
동남대학학보（의학판）
JOURNAL OF SOUTHEAST UNIVERSITY(MEDICAL SCIENCE EDITION)
2014年
2期
162-167
,共6页
方苏榕%谷伟%谭焰%孙丽华
方囌榕%穀偉%譚燄%孫麗華
방소용%곡위%담염%손려화
肺疾病,慢性阻塞性%克拉拉细胞分泌蛋白%噻托溴铵%炎症因子%大鼠
肺疾病,慢性阻塞性%剋拉拉細胞分泌蛋白%噻託溴銨%炎癥因子%大鼠
폐질병,만성조새성%극랍랍세포분비단백%새탁추안%염증인자%대서
chronic obstructive pulmonary disease%clara cell secretory protein%tiotropium bromide%inflammatory factors%rats
目的：探讨CC16在慢性阻塞性肺病（ COPD）发病机制中的作用。方法：将雄性SD大鼠随机分为健康对照组、COPD模型组（烟熏＋内毒素）和噻托溴铵药物干预组，每组10只。 RT-PCR检测各组大鼠气道上皮中CC16 mRNA的表达；免疫组化检测各组大鼠肺组织中CC16的蛋白表达；酶联免疫吸附试验（ ELISA ）检测各组大鼠血清中CC16、PLA2、IL8、TNFα的含量以及肺组织中PLA2、IL8、TNFα的含量。结果：大鼠气道上皮CC16 mRNA表达，COPD模型组较健康对照组显著减少，药物干预组较COPD模型组显著增加；血清及肺组织中CC16含量， COPD模型组较健康对照组显著减少，药物干预组较COPD模型组显著增加；血清及肺组织中PLA2、IL8、TNFα的含量，COPD模型组较健康对照组显著增多，药物干预组较COPD模型组显著减少（差异均有统计学意义，P＜0.05）。结论：在COPD大鼠形成过程中，气道上皮CC16 mRNA表达及肺组织CC16蛋白表达显著减少，这一改变可能是其小气道损伤的组织学标志，且与COPD的发生与发展有关。
目的：探討CC16在慢性阻塞性肺病（ COPD）髮病機製中的作用。方法：將雄性SD大鼠隨機分為健康對照組、COPD模型組（煙熏＋內毒素）和噻託溴銨藥物榦預組，每組10隻。 RT-PCR檢測各組大鼠氣道上皮中CC16 mRNA的錶達；免疫組化檢測各組大鼠肺組織中CC16的蛋白錶達；酶聯免疫吸附試驗（ ELISA ）檢測各組大鼠血清中CC16、PLA2、IL8、TNFα的含量以及肺組織中PLA2、IL8、TNFα的含量。結果：大鼠氣道上皮CC16 mRNA錶達，COPD模型組較健康對照組顯著減少，藥物榦預組較COPD模型組顯著增加；血清及肺組織中CC16含量， COPD模型組較健康對照組顯著減少，藥物榦預組較COPD模型組顯著增加；血清及肺組織中PLA2、IL8、TNFα的含量，COPD模型組較健康對照組顯著增多，藥物榦預組較COPD模型組顯著減少（差異均有統計學意義，P＜0.05）。結論：在COPD大鼠形成過程中，氣道上皮CC16 mRNA錶達及肺組織CC16蛋白錶達顯著減少，這一改變可能是其小氣道損傷的組織學標誌，且與COPD的髮生與髮展有關。
목적：탐토CC16재만성조새성폐병（ COPD）발병궤제중적작용。방법：장웅성SD대서수궤분위건강대조조、COPD모형조（연훈＋내독소）화새탁추안약물간예조，매조10지。 RT-PCR검측각조대서기도상피중CC16 mRNA적표체；면역조화검측각조대서폐조직중CC16적단백표체；매련면역흡부시험（ ELISA ）검측각조대서혈청중CC16、PLA2、IL8、TNFα적함량이급폐조직중PLA2、IL8、TNFα적함량。결과：대서기도상피CC16 mRNA표체，COPD모형조교건강대조조현저감소，약물간예조교COPD모형조현저증가；혈청급폐조직중CC16함량， COPD모형조교건강대조조현저감소，약물간예조교COPD모형조현저증가；혈청급폐조직중PLA2、IL8、TNFα적함량，COPD모형조교건강대조조현저증다，약물간예조교COPD모형조현저감소（차이균유통계학의의，P＜0.05）。결론：재COPD대서형성과정중，기도상피CC16 mRNA표체급폐조직CC16단백표체현저감소，저일개변가능시기소기도손상적조직학표지，차여COPD적발생여발전유관。
Objective:To explore the significance of CC 16 in the pathogenesis of chronic obstructive pulmonary disease( COPD ) by examining the CC16 expression in the airway epithelium of COPD rats before and after Tiotropium intervention.Methods: The male Sprague-Dawley(SD)rats were randomly assigned into the healthy control group , COPD model group ( smoke+endotoxin ) , and Tiotropium intervention group , with 10 in each .RT-PCR was used to detect the gene expression of CC 16 mRNA and immunohistochemistery was applied to test the protein expression of CC16 in the lung tissue in each group of rats .Enzyme-linked immunosorbent assay (ELISA) was adopted to investigate the levels of CC 16, PLA2, IL8 and TNFαin the serum as well as PLA2, IL8, and TNFαin the lung tissue .Results: CC16 mRNA gene expression was significantly reduced in the lung tissue of COPD model group compared with the healthy control group , but remarkably increased in Tiotropium intervention group as opposed to COPD model group .CC16 was found to be higher in the serum and lung tissue of COPD model group and PLA2, IL8 and TNFαwere lower than those in the healthy control group , while CC16 level was shown to be markedly elevated in the serum and lung tissue of Tiotropium intervention group and PLA 2, IL8, and TNFαlevels were significantly lower when compared with COPD model group .The differences were statistically significant (P<0.05).Conclusion:Gene expression of CC16 mRNA and CC16 protein expression in the airway epithelium decreased in the development of COPD rats , which may be a histological marker of mild airway injury in pathogenesis of COPD and involved in the development and progression of COPD .
