| Objective To establish an asthmatic model of mice sensitized with RSV,observe the effection of expression levels of MEK in Mouse Lung Tissue,study and observe pathological phenomenon change of Pingchuan Ⅰ in airway inflammation and airway remodeling of asthmatic mice.Methods Thirty-six healthy male BALB/C mice were divided into six groups,which were normal group,model group,dexamethasone group,Pingchuan Ⅰ low,middle and high-dose group,6 rats in each group.Mice were sensitized by the mixture with RSV and aluminum hydroxide,then inhaled with RSV to stimulate the airway to make asthmatic murine model.Mices were sacrificed within 24 hours after final stimulation,the right middle lobes of lung tissues were taken for HE staining to do pathologic investigation.Quantitative Real-time PCR and Western Blot were used to measure the lever of MEK mRNA and protein in the mouse’s lung tissues.The airway wall thickness(Wat/Pbm),bronchial smooth muscle thichness(Wam/Pbm)were measured by image analysis system.Analysis technique about linear correlation was used to measured the correlation between the Wat、Wam、MEK1/2 and MEK1、MEK2.Results Pathology observed under light microscope:Nrmal group occasionally very mild or no pathological damage.Asthma model group showed obvious pathological damage.Statistical analysis:Asthma model group Wat/Pbm,Wam/Pbm with the normal group,the treatment group difference was statistically significant(Average value of P<0.05);MEK1/2 gene and protein the results showed that the expression levels:The result of the model group comparison with that of the normal group and all treatment groups show(P<0.01,P<0.05)to comparative differences was significative;Pingchuan I dose group comparison with dexamethasone group,it was found to be significant(P<0.05),in which,the lever of the Pingchuan Ⅰ high dose group were lower than the dexamethasone group(P<0.05).Wat/Pbm and Wam/Pbm positively correlated with the MEK1/2(P<0.01).Conclusion It is more reliable to copy asthmatic model of mice with RSV inactivated.MEK1/2 plays an important role in pathogenesis of allergic asthma,adequate Pingchuan Ⅰ can lown the abnormal expression of MEK1/2.Pingchuan Ⅰ is able to inhibit the airway remodeling of asthmatic model of mice,the mechanism is may to inhibit the over expression of MEK1/2 to interrupt signal transduction of ERK to educe the airway remodeling of asthmatic miceobviously improving the symptoms. |