Objective:To investigate the effects of fluticasone on expression of basic fibroblast growth factor and mRNA in allergic rhinitis rats. Method:Ninety Sprague-Dawley rats were randomly divided into three groups(n = 30 for each) , including AR group, control group and fluticasone treatment group. In this experiment , the rat model of AR was established by the ovalbumin challenge methods. The expression of the protein of basic fibroblast growth factor and mRNA were detected with immunohistochemistry methods and in RT-PCR methods. Result:The protein and mRNA expression of basic fibroblast growth factor in nasal tissue was significantly higher in the AR group than that in control group(P<0.01),and it was much lower in the treatment group than that in the AR group(P<0.01) ibut still higher than that in the control group(P<0.01). The epithelial cell was the chief expression cell. Conclusion:The basic fibroblast growth factor participates in the pathogenesis of AR ,and inhaled fluticasone can significantly inhabit the expression of the protein and mRNA of basic fibroblast growth factor in the chronic stage of AR,thus preventing the airway remodeling.

OBJECTIVE: To investigate the effects of fluticasone on expression of basic fibroblast growth factor and mRNA in allergic rhinitis rats. METHOD: Ninety Sprague-Dawley rats were randomly divided into three groups(n = 30 for each), including AR group, control group and fluticasone treatment group. In this experiment, the rat model of AR was established by the ovalbumin challenge methods. The expression of the protein of basic fibroblast growth factor and mRNA were detected with immunohistochemistry methods and in RT-PCR methods. RESULT: The protein and mRNA expression of basic fibroblast growth factor in nasal tissue was significantly higher in the AR group than that in control group (P < 0.01), and it was much lower in the treatment group than that in the AR group (P < 0.01), but still higher than that in the control group (P < 0.01). The epithelial cell was the chief expression cell. CONCLUSION The basic fibroblast growth factor participates in the pathogenesis of AR, and inhaled fluticasone can significantly inhabit the expression of the protein and mRNA of basic fibroblast growth factor in the chronic stage of AR, thus preventing the airway remodeling.
Androstadienes ; pharmacology ; Animals ; Female ; Fibroblast Growth Factor 2 ; genetics ; metabolism ; Fluticasone ; Male ; Nasal Mucosa ; drug effects ; metabolism ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley ; Rhinitis, Allergic, Perennial ; genetics ; metabolism