Zhang Kui, Zhang Yin, Cheng Yi-Jiang, Lu Li
Fist Affiliated Hospital of Guiyang College of Traditional Chinese Medicine, Guiyang 550001, China.
Zhongguo Zhong Yao Za Zhi. 2008 Sep;33(18):2129-32.
To observe the effects of Jiajian Bufei Tang on expessions of nuclear factor-kappaB (NF-kappaB), metalloproteinase (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in the airway remodeling of COPD rat model with lung-Qi deficiency syndrome.
Make quantitative stimulation with tobacco, SO2 and papin to establish COPD rat model with lung-Qi deficiency syndrome. Sixty male rats were randomly divided into: normal group (N), model group (M), low dose treatment group (LT), medium dose treatment group (MT), high dose treatment group (HT), and glucocorticoid treatment group (GCT). To observe the lung histopathological features. To measure the thinknesses of the airway wall and smooth muscle layer of the small airway by means of image analyzer, The NF-kappaB activity and the protein expressions of MMP-9 and TIMP-1 were examined by immunohistochemical analysis.
The NF-kappaB activity and the protein expressions of MMP-9 and TIMP-1 in brouch and lung and the thinknesses of the airway wall and smooth muscle layer in the M group were significanthly higher than those in the N group (P<0.01). After treatment, the NF-kappaB activity and the protein expressions of MMP-9 in the HT, MT and GCT group were lower than those in the M group (P<0.01), the GCT group was better than the HT, MT group. The protein expressions of TIMP-1 in HT, MTgroup were lower than that in the M group. The thinknesses of the airway wall and smooth muscle layer were lower in the HT group than those in the M group (P<0.05).
Shenqi Bufei Tang may downregulate the NF-kappaB activity and the protein expressions of MMP-9 and TIMP-1 and intervene in the airway remodeling of COPD rat model with lung-Qi deficiency syndrome.
观察加减补肺汤对慢性阻塞性肺疾病（COPD）肺气虚证大鼠模型气道重塑中核因子-κB（NF-κB）、基质金属蛋白酶（MMP-9）及基质金属蛋白酶组织抑制因子-1（TIMP-1）表达的影响。
采用烟草、二氧化硫及木瓜蛋白酶定量刺激建立COPD肺气虚证大鼠模型。将60只雄性大鼠随机分为：正常组（N）、模型组（M）、低剂量治疗组（LT）、中剂量治疗组（MT）、高剂量治疗组（HT）及糖皮质激素治疗组（GCT）。观察肺组织病理特征。用图像分析仪测量小气道气道壁及平滑肌层厚度，采用免疫组化分析法检测NF-κB活性及MMP-9和TIMP-1蛋白表达。
M组支气管及肺组织中NF-κB活性、MMP-9和TIMP-1蛋白表达以及气道壁和平滑肌层厚度均显著高于N组（P<0.01）。治疗后，HT组、MT组及GCT组NF-κB活性和MMP-9蛋白表达低于M组（P<0.01），GCT组优于HT组、MT组。HT组、MT组TIMP-1蛋白表达低于M组。HT组气道壁和平滑肌层厚度低于M组（P<0.05）。
参芪补肺汤可能下调NF-κB活性及MMP-9和TIMP-1蛋白表达，干预COPD肺气虚证大鼠模型气道重塑。
