摘要
目的观察N-乙酰半胱氨酸(NAC)、红霉素和地塞米松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。将大鼠随机分为正常对照组、COPD组、NAC组、红霉素组和地塞米松组,每组10只。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法检测各组大鼠肺组织中CC16 mRNA的含量。结果COPD组大鼠终末细支管上皮Clara细胞占上皮细胞的百分比明显低于对照组,差异有显著性(P<0.01);NAC组和红霉素组Clara细胞百分比与COPD组相比有所增加(分别为P<0.01,P<0.05);而地塞米松组与COPD组无统计学差异(P>0.05)。COPD组大鼠BALF和血清中CC16蛋白水平(A)明显低于对照组,差异有显著性(P<0.01);NAC组及红霉素组BALF和血清中CC16蛋白水平明显高于COPD组,差异也有显著性(P<0.05);而地塞米松组大鼠BALF和血清中CC16蛋白水平与COPD组比较差异无显著性(P>0.05)。COPD组大鼠肺组织中CC16 mRNA的含量明显低于对照组,NAC干预组和红霉素组明显高于COPD组(分别为P<0.01,P<0.05),而地塞米松组与COPD组比较差异无显著性(P>0.05)。结论被动吸烟所致COPD大鼠的慢性气道炎症可导致Clara细胞数量及CC16的合成及分泌量减少,NAC和红霉素可能通过促进CC16的合成和分泌抑制气道炎症反应,地塞米松对CC16的合成及分泌量未见明显影响。
Objective To investigate the effects of N-acetylcysteine （NAC）, erythromycin （ETM） and dexamethasone （DEX） on the number of Clara cells and secretion of Clara cell secretory protein （CC16） in rat chronic obstructive pulmonary disease （COPD） model. Methods Fifty rats were divided into control, COPD, NAC, ETM and DEX groups （n = 1 0）. The number of Clara cells was detected by immunohistochemistry. The CC16 level in bronchoalveolar lavage fluid （BALF） and serum was detected by ELISA. The level of CC16 mRNA in the lung was detected by RT-PCR. Results The percentage of Clara cells in terminal bronchioles in the rats of COPD group was significantly lower than that in the control （ P 〈 0.01 ）, and the percentages of Clara cells in NAC and ETM groups were significantly higher than that in the COPD group （ P 〈 0.01, P 〈 0.05, respectively）. But there was no significant difference between DEX and COPD groups in the percentage of Clara cells. The level of CC16 in the BALF and serum in the COPD group was significantly lower than that in the control group （P 〈 0.01 ） ,and that in NAC and ETM groups were significantly higher than that in the COPD group （ P 〈 0.05）. But there was no significant difference between levels of CC16 in BALF and serum in the DEX and COPD groups. The expression of the lung CC16 mRNA in COPD group was weaker than that in the control group, and that in NAC and ETM groups was significantly higher than that in the COPD group （P 〈 0.01, respectively）. There was no significant difference between expressions of the lung CC16 mRNA in the DEX and COPD groups （P 〉 0.05 ）. Conclusion The number of Clara cells and the secretion of CC16 are reduced in the rat COPD model. NAC and ETM can elevate the synthesis and secretion of CC16, Which may be a mechanism for their suppression of airway inflammation. There is no significant effect of DEX on CC16 in the COPD rat model.
出处
《中国比较医学杂志》
CAS
2008年第2期1-4,F0003,共5页
Chinese Journal of Comparative Medicine
