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目的:探讨丙酸氟替卡松对哮喘小鼠气道重塑的影响及其可能的作用机制.方法:将30只Balb/c小鼠随机分为哮喘组(A组),正常对照组(B组),丙酸氟替卡松治疗组(C组)3组,每组动物l0只.A组小鼠于第1日及第15日以鸡卵白蛋白(OVA)致敏,从第1次致敏后第22日开始雾化吸入25g/LOVA激发并持续4wk,建立哮喘气道重塑模型;B组用生理盐水以同样方法致敏并雾化吸入;C组于激发前30min雾化吸入丙酸氟替卡松(0.17g/L),吸入时间每次10min,其它程序与A组相同.制备小鼠肺组织病理切片,HE染色观察各组气道结构改变情况,采用医学图像分析软件测定支气管管壁厚度(WAt/Pbm),支气管平滑肌厚度(WAm/Pbm);肺组织石蜡切片行TGF-β1免疫组化染色后计算机图像分析测定其灰度值.结果:光镜下可见A组小支气管上皮细胞脱落、管壁炎症细胞浸润、杯状细胞增生、平滑肌增厚,而C组上述改变较A组明显减轻.与B组比较,A组支气管管壁厚度[(17.43±1.10)μm2/μm],平滑肌厚度[(6.58±1.16)μm2/μm]显著升高(P<0.01);与A组比较,C组支气管管壁厚度[(14.06±1.20)μm2/μm],平滑肌厚度[(4.41±1.00)μm2/μm]显著降低(P<0.01).与B组比较,A组TGF-β1的灰度值(66.18±1.53)显著降低(P<0.01);与A组比较,C组丙酸氟替卡松干预后TGF-β1的灰度值(72.05±1.65)显著升高(P<0.01).结论:吸入丙酸氟替卡松能有效防治哮喘小鼠气道重塑,可能的机制是丙酸氟替卡松通过下调TGF-β1的表达干预了气道重塑.
Objective: To investigate the effect of fluticasone propionate on airway remodeling in asthmatic mice and its possible mechanism.Methods: Thirty Balb / c mice were randomly divided into asthma group (A group), normal control group (B group) , Fluticasone propionate treatment group (C group) 3 groups, l0 mice in each group.A group of mice on the 1st and 15th day with chicken ovalbumin (OVA) sensitized from the first sensitized after the first 22 At the beginning of aerosol inhalation, 25g / LOVA was stimulated for 4wk to establish the airway remodeling model of asthma. Group B was sensitized and inhaled by the same method with saline. In group C, fluticasone propionate (0.17 g / L), inhalation time was 10min each time, and the other procedures were the same as that of group A. The pathological sections of lung were prepared and the changes of airway structure were observed by HE staining. The thickness of bronchial wall was measured by medical image analysis software (WAt / Pbm) and bronchial smooth muscle thickness (WAm / Pbm) .The lung tissue paraffin sections were subjected to immunohistochemical staining for TGF-β1 and the gray value of TGF-β1 was detected by computer image analysis.Results: The bronchial epithelial cells in group A were shed by light microscope, Inflammatory cell infiltration, goblet cell hyperplasia, smooth muscle thickening, while the above changes in group C were significantly reduced compared with group A. Compared with group B Compared with group A, the thickness of bronchial wall in group A was significantly higher than that in group A ([(17.43 ± 1.10) μm2 / μm] and thickness of smooth muscle [(6.58 ± 1.16) μm2 / μm] Compared with group B, the gray value of TGF-β1 in group A (66.18 ± 1.53) was significantly lower than that in group B [(14.06 ± 1.20) μm2 / μm] and smooth muscle thickness [(4.41 ± 1.00) μm2 / (P <0.01) .Compared with group A, the gray value of TGF-β1 (72.05 ± 1.65) in group C was significantly increased after fluticasone propionate intervention (P0.01) .Conclusion: Fluticasone propionate inhalation is effective To prevent airway remodeling in asthmatic mice, the possible mechanism is that fluticasone propionate interferes with airway remodeling by down-regulating the expression of TGF-β1.