Influence Of Aquporin On The Expression And Secretion Of Mucins In Rat Of Airway Hyperresponsiveness

Objective:Airway hypellresponsiveness(AHR)refers to a variety Of physical, chemical, airway allergen or movement were highly sensitive state.①this experiment from the airway destabilization mechanism ot ozone stress rats, establishing airway hyperresponsiveness models, and detection of the animal model of stability and reliability:②observation of ozone stress in rats lung tissue aquaporin(AQP)expression in airway hyperresponsiveness, analysis of abnormal expression of AQPs;③obser-ve ozone stress after bronchial secretion of mucin aggregates, lung tissue mucin gene MUC5AC expression is altered and abnormal expression of AQPs change, explore the abnormal expression of AQPs on ozone stress rat airway mucus secretion the quantity and quality effects.Methods:①20SD rats were randomly divided into2groups:normal control group; ozone stress group with10rats in each group. Detection of the animal model of expiratory airway resistance(Re), bronchoalveolar lavage fluid cell count, classification, total protein content, pulmonary, bronchial biopsy and clear index the model stability and reliability;②20SD rats were randomly divided into2groups:normal control group; groups of ozone stress10only. Using real time fluorescent quantitative RT-PCR and Western Blot detection of ozone stress in pulmonary tissue after three AQPs(AQP1, AQP4, AQP5) expression in airway hyperresponsiveness, analysis of abnormal expression of AQPs;③30SD rats were randomly divided into3groups: normal control group; ozone stress group; ozone stress and dexamethasone in treatment group,10rats in each group. Packet detection of bronchial secretion of mucin aggregates, lung tissue mucin gene MUC5AC expression change and ozone stress in lung tissue after three kinds of abnormal expression of AQPs(AQP1, AQP4, AQP5)volume, analysis of the correlation between them.Results:①Using exogenous injury factor of ozone(ozone, O3)attack of bronchial epithelial cells formed airway hyperresponsiveness models each index(airway reactivity,bronchoalveolar lavage fluid cell count, classification, total protein content determination, pulmonary, bronchial biopsy)were confirmed by determination of airway hyperresponsiveness in existence;②rat lung tissue AQP1, AQP4, AQP5and AQP5were expressed, expression of most; ozone stress on airway hyperresponsiveness in rats after AQP1, AQP4, AQP5expression was significantly decreased;③in the lung tissue of rats with MUC5AC expression, ozone stress after a few days, the rat airway, mucus secretion increased significantly, and the expression of MUC5AC increased, the two positive correlation trend.④With AQPs down-regulates, high reaction of airway mucus secretion in rats increased significantly, MUC5AC expression. Tip AQPs expression and airway mucus secretion gross present negative correlation; the expression of AQPs and mucus in MUC5AC expression negative trend.Conclusion:Exogenous injury factor O3attack of bronchial epithelial cells, airway epithelial cell function defect or loss of homeostasis, onset of airway hyperresponsiveness. In the process of airway hyperresponsiveness, mucus hypersecretion and expression levels of MUC5AC, AQPs down-regulates increased bronchial mucus secretion and MUC5AC expression. Our analysis that the AQP1, AQP4, AQP5may lead to decreased airway hyperresponsiveness of lung water in capillaries and alveolar interstitial transport imbalance, exacerbations of airway inflammation, the release of a variety of inflammatory mediators, the ciliary epithelium and goblet cell ratio imbalance, eventually leading to water obstacle clearance, mucus hypersecretion.