强肌健力方对肺脾两虚型COPD大鼠气道壁厚度和转移生长因子β1的影响

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目的:观察肺脾两虚型COPD大鼠模型气道重塑、TGF-β1的表达,以及强肌健力方对气道壁厚度及TGF-β1表达的影响。方法:利用烟熏和气道内2次滴入脂多糖合并番泻叶冷服泻下法复制肺脾两虚型COPD大鼠模型。采用随机平行对照的实验方法,将40只SD大鼠随机分为强高组、强低组、模型组和正常组4组,每组各10只。造模结束后,取各组大鼠肺组织切片行HE染色,光镜下观察病理改变,并用测微尺测量气管壁厚度,采用荧光定量PCR法检测肺组织TGF-β1 cDNA的含量。结果:模型组基本符合人类COPD病理生理变化。模型组气道壁厚度较正常组明显增厚(P<0.05),强高组气道壁厚度明显变薄,与模型组比较有显著性差异(P<0.05),但强低组与模型组比较无明显变化(P>0.05)。模型组肺组织TGF-β1 cDNA含量较正常组明显升高(P<0.01),强高组、强低组肺组织TGF-β1 cDNA含量明显降低,与模型组比较有显著性差异(P均<0.01),但强高、强低组组间比较无显著性差异(P>0.05)。结论:慢性烟熏和气道内滴入LPS合并番泻叶冷服泻下法能构建含有气道重塑特征的肺脾两虚型COPD大鼠模型;强肌健力方能抑制肺脾两虚型COPD大鼠TGF-β1的表达,减轻气道炎症,减少气道壁厚度的增加。 OBJECTIVE: To observe the airway remodeling and expression of TGF-β1 in lung and spleen deficient COPD rat models, and the effect of Qiangji Jianli Fang on airway wall thickness and TGF-β1 expression. Methods: The lung and spleen deficiency COPD rat models were duplicated by smoking and intratracheal instillation of lipopolysaccharide twice and cold diarrhea underwent diarrhea. Using randomized parallel experimental methods, 40 SD rats were randomly divided into 4 groups: strong high group, strong low group, model group and normal group, 10 in each group. After the completion of the model, the lung tissue sections of each group were stained with HE, the pathological changes were observed under a light microscope, and the thickness of the tracheal wall was measured with a micrometer. The content of TGF-β1 cDNA in lung tissue was detected by fluorescent quantitative PCR. Results: The model group basically met the pathophysiological changes of human COPD. The airway wall thickness in the model group was significantly thicker than that in the normal group (P<0.05). The thickness of the airway wall in the strong high group was significantly thinner (P<0.05), but the strong and low group and the model group were significantly different. There was no significant change (P>0.05). The TGF-β1 cDNA content in the lungs of the model group was significantly higher than that in the normal group (P<0.01), and the TGF-β1 cDNA content in the lungs of the strong high group and the low-dose group was significantly decreased, and there was a significant difference compared with the model group (P< 0.01), but there was no significant difference between the high-strong and low-low groups (P>0.05). Conclusion: Chronic lung smoke and LPS instillation in the airway combined with senna leaf cold diarrhea method can construct a lung and spleen deficiency type COPD rat model with airway remodeling; Qiangji Jianli can inhibit the deficiency of lung and spleen. The expression of TGF-β1 in COPD rats reduced airway inflammation and decreased airway wall thickness.
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