ObjectiveTo study YiFeiJianPi Prescription prevention and treatment of chronic obstructivepulmonary disease rat model of airway inflammation and airway mucus hypersecretion effect.MethodsIntratracheal injection of LPS method and Smokedto establish COPD model.The40male SD rats were randomly divided into four groups,10/group,they are normal control group,COPD model group,simvastatin treatment group, YiQiJianPi treatment group.Using thepulmonary function testing instrument to test pulmonary function of the rats, Using themethod of HE staining to observe the rats,lung and bronchus pathological changes,and measure the thickness of each rat tracheal wall and tracheal smooth muscle.To usethe Enzyme-linked immunosorbent assay to detect the alveolar lavage fluid of IL-8,IL-17, TNF-α, MMP-9levels. Alcian blue-periodic acid Schiff staining airway gobletcells.Immunohistochemistry was used to detect rats’ lung tissue NF-κB,ICAM-1,MUC5ac and TLR4protein expression. Western-blot method is used to detectMUC5ac and TLR4protein content in rats’ airway.Fluorescence quantitative RT-PCRmethod is used to detect the expression of TLR4mRNA and MUC5acmRNA in lungtissue.ResultsCompared with normal control group, the lung function of Simvastatin treatmentgroup and YiQiJianPi treatment group significantly decreased;compared with theCOPD group, simvastatin is compared with YiQiJianPi, in the factor of improvingFVC, the former’s effect is significant (P<0.01), in improving FEV0.1andFEV0.1/FVC, the latter’s effect is significant (P<0.01).The rats of COPD modelgroup,s Bronchial and lung tissue HE staining comply with COPD lung tissuepathology.Simvastatin treatment group and YiQiJianPi treatment group in comparedwith normal control group, there are different degrees of lung tissue damage, but compared with the COPD group, the degree of injury significantly reduced.Simvastatin group and YiQiJianPi treatment group rats,s airway wall thickness andairway smooth muscle thickness increased compared with the normal control group,compared with the model group, but also significantly reduced (P<0.01). Simvastatin iscompared with YiQiJianPi, the former in terms of inhibiting airway wall thickening,the effect was significantly better than the latter (P<0.01). COPD model group inBALF IL-8, IL-17, TNF-α, MMP-9were significantly higher levels than normalcontrol group (P<0.01), simvastatin group and YiQiJianPi treatment group in comparedwith COPD model group ratio, which were significantly lower (P<0.01), but stillhigher than the normal control group (P<0.01); In reducing IL-8, MMP-9levels, theeffect of simvastatin is more significant (P<0.01); in reducing TNF-α levels,YiQiJianPi is more effective than simvastatin (P<0.01).COPD model rats airwayICAM-1, NF-κB, MUC5ac and TLR4protein expression was significantly increased(P<0.01),Simvastatin group and YiQiJianPi treatment group in compared with COPDmodel group, ICAM-1, NF-κB, MUC5ac and TLR4protein expression levels weresignificantly lower (P<0.01), but still higher than the normal control group (P<0.01).Simvastatin is compared with YiQiJianPi, in reducing the relative expression levelsand protein expression levels of MUC5ac, simvastatin’s effect is much better thanYiQiJianPi (P<0.05), but in terms of reducing MUC5acmRNA expression, both notstatistically significant (P>0.05).ConclusionSimvastatin and YiQiJianPi Prescription can significantly improve the lungfunction and chronic obstructive pulmonary disease pathological damage in rats,reduce the levels of IL-8, IL-17, TNF-α, MMP-9in BALF of COPD rat model, inhibitlung tissue ICAM-1, NF-κB, MUC5ac and TLR4protein content,by reducingairway inflammation and airway mucus hypersecretion role to achieve the purpose ofprevention. |