论文部分内容阅读
目的:观察慢性阻塞性肺病(COPD)大鼠肺组织局部树突状细胞(DC)的存在状况,并探讨吸入糖皮质激素布地奈德及抗胆碱能受体支气管扩张剂异丙托溴铵对COPD大鼠肺部DC数目的影响。方法:60只健康雄性SD大鼠随机分为4组(n=15):正常对照组、COPD模型组、布地奈德组、异丙托溴铵组。后3组用两次气管内注入脂多糖(LPS,200μg/只)及熏香烟4周的复合刺激法建立大鼠COPD模型,布地奈德组、异丙托溴铵组于第8天起每天吸入相应药液。于第31天处死,肺组织切片H-E染色观察病理改变,免疫组化染色观察DC的表达。结果:COPD模型组、布地奈德组、异丙托溴铵组均出现COPD的特征性病理改变,且肺组织内DC的数量明显高于正常对照组,差异有统计学意义(P<0.01);布地奈德组DC数目则较COPD模型组明显减少(P<0.01),异丙托溴铵组DC数目与COPD模型组比较差异无统计学意义。结论:DC在COPD的发病机制中有重要作用,糖皮质激素布地奈德干预可以降低COPD大鼠肺部DC的数量,异丙托溴铵则无此作用。
OBJECTIVE: To observe the presence of local dendritic cells (DCs) in the lung tissue of chronic obstructive pulmonary disease (COPD) rats and to investigate the effects of inhaled glucocorticoid budesonide and anticholinergic bronchodilator ipratropium bromide On the number of pulmonary DC in COPD rats. Methods: Sixty healthy male SD rats were randomly divided into 4 groups (n = 15): normal control group, COPD model group, budesonide group and ipratropium bromide group. The rats in the latter 3 groups were given COPD model by double-intratracheal instillation of LPS (200μg / body) and smoked cigarettes for 4 weeks. Budesonide group and ipratropium group Inhalation of the corresponding liquid. The rats were killed on the 31st day. The pathological changes were observed by H-E staining and the expression of DC was observed by immunohistochemistry. Results: The pathological changes of COPD were observed in COPD model group, budesonide group and ipratropium bromide group, and the number of DC in lung tissue was significantly higher than that in normal control group (P <0.01) ; While the number of DC in budesonide group was significantly lower than that in COPD model group (P <0.01). There was no significant difference in the number of DC between ipratropium bromide group and COPD model group. CONCLUSION: DC plays an important role in the pathogenesis of COPD. Budesonide, a glucocorticoid, can reduce the number of DCs in the lungs of COPD rats, while ipratropium bromide does not.