摘要
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.
AIM: To investigate the influence of flutieasone propionate (FP)on airway remodeling in murine models of asthma and its mechnisms. METHODS: Thirty Balb/c mice were randomly divided into 3 groups: model group (group A ), normal control group(group B), FP treatment group(group C), with 10 mice in each group. Group A were sensitized on day 1 and 15 by ovalbumin(OVA) and challenged from day 22 to 49 by repeated OVA inhalation (25 g/L per day ) to establish murine models of asthma characterized by airway inflammation and airway remodeling. Group B were sensitized and challenged by normal saline with the same method. Group C were challenged with FP (0. 17 g/L per day) 30 min before OVA challenge as group A did. The airway inflammation and the 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: Bronchial epithelial desquamation, inflammatory cell infiltration, hyperplasia of goblet cells and smooth muscle cells were seen in group A under optical microscope, however compared with group A, the manifes- tations were significantly decreased in group C. Compared with group B, WAm/Pbm [ ( 17.43 ± 1.10) μm^2/μm] and WAt/ Pbm [ (6.58 ± 1.16)μm^2/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) μm^2/μm ] and WAt/Pbm [ (4.41 ± 1.00)μm^2/μm ] were expressed at lower levels in lung tissues of group C( P 〈 0.01 ) . Compared with group B, the gray value of TGF-β1 in group A ( 66.18 ± 1.53 ) was lower ( P 〈 0.01 ), however it decreased significantly in group C ( 72.05 ± 1.65 ) when compared with that in group A ( P 〈 0. 01 ). CONCLUSION: The airway remodeling can be inhibited by FP probably throughreducing the expression of TGF-β1.
出处
《第四军医大学学报》
北大核心
2007年第12期1088-1090,共3页
Journal of the Fourth Military Medical University
关键词
丙酸氟替卡松
哮喘
气道重塑
转化生长因子Β
fluticasone propionate
asthma
airway remodeling
transforming growth factor beta
mice