【摘要】 目的观察参芪补肺汤对慢性阻塞性肺疾病(COPD)肺气虚证大鼠支气管平滑肌(ASM)增殖中组蛋白去乙酰化酶-2(HDAC2)和核因子κB(NF-κB)p65表达的影响。方法将40只SD雄性大鼠随机分为正常对照组、模型对照组、参芪补肺汤组、氨茶碱组,每组各10只。采用气管内滴注脂多糖加烟熏28 d的方法建立COPD肺气虚证模型。光镜下观察肺组织病理形态学变化,图像分析法测量小气道管壁和ASM厚度,采用免疫组化、实时荧光定量PCR和Wester blot方法检测大鼠ASM中HDAC2和NF-κB p65表达。结果与正常对照组比较,模型对照组大鼠气道管壁和ASM明显增厚(P<0.05),NF-κB p65 mRNA和蛋白表达明显增高(P<0.05),HDAC2 mRNA和蛋白表达明显降低(P<0.05)。与模型对照组比较,参芪补肺汤组和氨茶碱组气道管壁和ASM厚度明显降低(P<0.05),NF-κB p65 mRNA和蛋白表达明显降低(P<0.05),HDAC2mRNA和蛋白表达均明显升高(P<0.05),参芪补肺汤组与氨茶碱组比较,均差异无统计学意义(P>0.05)。结论参芪补肺汤可抑制COPD肺气虚证模型大鼠ASM增殖,其机制与其提高HDAC2表达、减少NF-κB p65表达有关。更多还原

【Abstract】 Objective To examine the effects of Shenqi Bufei Tang decoction on the expression of histone deacetylase-2( HDAC2) and nuclear factor-κB p65( NF-κB p65) in the airway smooth muscle tissues of COPD rats with lung-qi deficiency syndrome. Methods A total of 40 male rats were randomly divided into normal control group,model control group,Shenqi Bufei Tang decoction group,and aminophylline group.The COPD rat model with lung-qi deficiency syndrome was established by intratracheal instillation of lipopolysaccharide( LPS) and passive smoking for 28 days. Pathological changes of lung tissues were observed under the light microscope and the thickness of the small airway wall and airway smooth muscle( ASM) layer analyzed by the image analysis.Immunohistochemistry,real-time PCR and Western blotting were used to detect the expressions of NF-κB p65 and HDAC2 in ASM. Results The thickness of the airway wall and ASM,and the expression levels of NF-κB p65 mRNA and protein were significantly increased in the model control group when compared with those in the normal control group( P<0.05).They were significantly reduced and the expression levels of HDAC2 mRNA and protein were markedly increased in Shenqi Bufei Tang decoction group and aminophylline group,which were compared with those in the model group( P<0.05).There were no significant differences in these indices between Shenqi Bufei Tang decoction group and aminophylline group( P> 0.05). Conclusion Shenqi Bufei Tang decoction can inhibit the proliferation of ASM in COPD rats with lung-qi deficiency syndrome,which may be associated with the increased expression of HDAC2 and decreased expression of NF-κB p65.更多还原