Effect Of Fluticasone Propionat On Airway Remodeling And The Expression Of Transforming Growth Factor-β₁ In A Murine ModeI Of Asthma

Asthma is a kind of chronic airway inflammation.More and more testimonies have shown that asthma involves not only airway inflammation and nonspecific hyperactivity ,but also airway wall remodeling(AWR). AWR is an important pathologic character of asthma. Maybe it can cause irreversibal airway obstruction and persistent hyperactivity.Probably it is pathologic foundation of refractory asthma's repeated attack. Its mechnisms is complex.Many factors participate in the process of AWR in asthma ,including cells, cytokines and inflammmatory mediaters .Generally many literates think that AWR is caused by partial or hypernomic restoration. Effectively controlling airway inflammation and preventing AWR is the key of therapy of asthma .Presently inhaled corticosteroids(ICS) is the most effective antiphlogist on about therapy of asthma,but whether ICS can prevent and cure AWR is not clear. Fluticasone propionat(FP) is one of the new fatsoluble glucocorticoid. It has high affinity for glucocorticoidreceptor(GR).Its oral bioavailability is less than one percent. The ability of antiinflammation is twelve times more than that of budesonide(BUD) and twenty times more than that of bedomethasone(BDP). FP has been used widely.Studyies about the influence of FP on airway remodeling are few.The murine model of asthma was used in the study to investigate the effect of FP on the airway wall thickness,the bronchial smooth muscle thickness and the expression of transforming growth factor-β1 and to investigate the influence of FP on airway remodeling in murine models of asthma and its mechanisms.Methods :⑴Establish murine models of asthma characterized by airway inflammation and airway remodeling.⑵Thirty BALB/c mice were randomly divided into 3 groups:the model group(group A),the normal group(group B), the treatment group(group C), with 10 mice in each group. The characteristic airway inflammation and alteration of airway structure were detected by HE staining. The airway wall thickness(WAt/ Pbm),the bronchial smooth muscle thickness(WAm/Pbm) were measured by using image analysis system.Pulmonary expression and location of transforming growth factor-β1(TGF-β1)were examined by immunohistochemistry.Results: ⒈After asthmatic models of murine inhaled ovalbumin for four weeks, bronchial submucosa broadening, bronchial epithelial desquamation, hyperplasia of goblet cells and smooth muscle cells were seen under optical microscope.⒉⑴Bronchial epithelial desquamation, inflammator cells infiltration, hyperplasia of goblet cells and smooth muscle cells were seen in group A under optical microscope. However compared with group A, those manifestations were significantly attenuated in group C.⑵Compared with group B,WAm/Pbm [(17.43±1.10)μm2/μm] and WAt/Pbm [(6.58±1.16)μm2/μm ]were expressed at higher levels in lung tissues of group A(P<0.01); Compared with group A, WAm/Pbm[ ( 14.06±1.20 )μm2/μm ]and WAt/Pbm [(4.41±1.00)μm2/μm] were expressed at lower levels in lung tissues of group C(P<0.01) .⒊Compared with group B, the gray value of TGF-βl in group A(66.18±1.51) was lower, (P<0.01), however it decreased significantly in group C(72.05±1.65)when compared with that in group A.Conclusion:⑴After asthmatic models of murine inhaled ovalbumin for four weeks,airway remodeling models were established.⑵The airway remodeling can be partially inhibited by FP,.⑶TGF-β1 participate in the process of AWR in asthma. FP may be inhibite the airway remodeling by reducing the expression of TGF-β1 .