摘要
目的:观察抗氧化剂N-乙酰半胱氨酸(NAC)干预对大鼠慢性阻塞性肺疾病(COPD)模型Clara细胞数量及其分泌蛋白CC16表达的影响。方法:单纯熏香烟法建立Wistar大鼠COPD模型。将大鼠随机分为对照组、COPD组和NAC干预组,每组10只。应用透射电镜观察COPD大鼠肺组织Clara细胞超微结构的变化。免疫组织化学方法检测各组大鼠肺组织Clara细胞数量。酶联免疫吸附法检测支气管肺泡灌洗液(BALF)和血清中CC16含量。RT-PCR法检测肺组织中CC16mRNA的含量。结果:COPD组大鼠终末细支气管上皮Clara细胞占上皮细胞的百分比明显低于对照组(P<0.01);NAC干预组明显高于COPD组(P<0.01)。COPD组大鼠BALF和血清中CC16蛋白水平明显低于对照组(P<0.01);NAC干预组明显高于COPD组(P<0.05)。COPD组大鼠肺组织中CC16mRNA的含量明显低于对照组和NAC干预组(均P<0.01)。结论:COPD大鼠的气道炎症可导致Clara细胞数量及CC16的合成及分泌量减少,抗氧化剂NAC可通过促进CC16的合成和分泌抑制气道炎症反应。
AIM ： To investigate the effects of N - acetylcysteine （NAC） on the number of Clara cells and secretion of Clara cells secretory protein （CC16） in rat chrohic obstructive pulmonary disesae （COPD） model. METHODS： Thirty rats were divided into control, COPD and NAC groups （n = 10）. The change of Clara cell ultrastructure was detected through transmission electron microscope. The number of Clara cells and synthesis of CC16 were measured by immunohistochemistry, The CC16 levels in bronchoalveolar lavage fluid （BALF） and serum were tested by ELISA. The level of CC16 mRNA in lung was determined by RT - PCR. RESULTS： The percentage of Clara cells in terminal bronchioles in the COPD group was significantly decreased than that in the control （P 〈0. 01 ）, and the percentage in NAC group was significantly higher than that in COPD group （ P 〈 0. 01 ）. The levels of CC16 in the BALF and serum in COPD group were significantly lower than those in control group （P 〈 0.01, respectively）, and the levels of CC16 in NAC group were significantly higher than those in COPD group （P 〈 0. 05, respectively）. The expression of CC16 mRNA in COPD group was weaker than that in control group and NAC group （P 〈0. 01, respectively）. CONCLUSION： The number of Clara cells and the secretion of CC16 decrease in a rat model of COPD. Antioxidant NAC can enhance the synthesis and secretion of CC16, which may be a mechanism for the suppression of airway inflammation.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2008年第1期20-23,共4页
Chinese Journal of Pathophysiology
基金
山西医科大学学生创新项目基金(No.2004009)
