加味小青龙汤对慢性阻塞性肺疾病大鼠肺组织核转录因子-κB、锌指蛋白A20表达的影响

Effects of modified Xiaoqinglong Decoction on the expression of nuclear transcription factor-κB and zinc protein A20 in lung tissue of rats with chronic obstructive pulmonary disease

目的:观察加味小青龙汤对慢性阻塞性肺疾病(COPD)大鼠肺组织核转录因子-κB 65(NF-κB65)、锌指蛋白A20蛋白及其基因表达的影响。方法:Wistar大鼠按随机数字表法分为正常组、模型组、地塞米松和加味小青龙汤组。采用脂多糖气管滴注联合烟熏方法建立COPD大鼠模型,检测支气管肺泡灌洗液中TNF-α、IL-1β含量,检测肺组织NF-κB65、A20蛋白及其基因表达,观察加味小青龙汤对上述指标及肺组织病理形态学变化的影响。结果:与正常组比较,模型组TNF-α、IL-1β、NF-κB和A20蛋白及其基因表达均明显上调;与模型组比较,加味小青龙汤组TNF-α、白介素-1β、NF-κB蛋白表达明显降低,加味小青龙汤组A20基因表达显著上调。病理观察结果显示,与正常组比较,模型组肺组织炎症细胞浸润,管腔中有大量中性粒细胞及黏液聚集,管壁明显增厚,胶原染色显示肺间质纤维组织大量增生;加味小青龙汤组肺组织病理改变明显轻于模型组,加味小青龙汤组肺组织少数呈轻度间质性肺炎,仅见少量的纤维组织增生。结论:加味小青龙汤能够减轻COPD模型大鼠肺组织损伤,对COPD模型肺组织有保护作用,其机理可能与其降低TNF-α和白介素-1β含量、下调NF-κB蛋白表达、上调A20基因表达有关。

Objective： To investigate Effects of Additional Xiao Qing Long Decoction（ AXQLD） on Lung Expression of NF-k Bp65 and A20 protein and its mRNA in rats with chronic obstructive pulmonary disease（ COPD）.Methods： Wistar rats was randomly divided into normal control group,model control group. The COPD model of rats were bulit by the Lipopolysaccharide tracheal instillation and smudging. TNF-α and L-1 β in the bronchoalevlar lavage fluid were measured,and the expression of NF-κB and A20 protein and its mRNA in lung tissue were measured. While the histopathology of the lung tissue was observed by light microscope. Results： Compared with the normal control group,TNF-α and IL-1 β and the expression of NF-κB,A20 protein and its mRNA were obviously increased in model group. Compared with model group,TNF-α and IL-1 β and the expression of NF-κB protein were obviously decreased in AXQLD group; The expression of A20 mRNA was obviously increased in AXQLD group. Light microscope observation indicates that there were severe interstitial pneumonia, the destruction or disappearance of alveolar structure,the infiltration of the inflammatory cells, pulmonary interstitial fibrous tissue hyperplasia with great quantities in the model group. while the pathological manifestations were much more ameliorated than those of the model group,the mild interstitial pneumonia and only a small amount of fibrous tissue hyperplasia were showed in the AXQLD. Conclusion： AXQLD lessens the injury of lung tissue and has protective effects on COPD rats,the mechanism is possibly related to the inhibition of TNF-α,IL-1 β,and down-regulatation the expression of NF-κB protein and up-regulatation the expression A20 mRNA in COPD rats.