【摘要】 目的建立哮喘小鼠气道重构模型,观察孟鲁司特对哮喘小鼠气道重构的影响,探讨其机制。方法建模成功后,将动物分为四组:孟鲁司特(MK)干预组,激素(DXM)干预组、阴性对照组,阳性对照组。HE染色及阿尔新兰染色,分别观察支气管上皮细胞及粘液分泌情况。图像分析软件测定支气管平滑肌厚度确定不同组别气道重构程度。采用半定量PCR法检测小鼠精氨酸酶-Ⅱm RNA水平。结果 (1)阳性组出现粘液分泌增加、炎症细胞浸润、管壁增厚、平滑肌增生等,精氨酸酶-Ⅱm RNA水平增高;(2)MK组、DXM组炎症反应轻微,粘液分泌、平滑肌增生不明显。与阳性组比较,MK组、DXM组精氨酸酶-Ⅱm RNA水平降低;差异有统计学意义。结论发生气道重构哮喘小鼠的精氨酸酶-Ⅱ表达水平升高,MK干预可降低精氨酸酶-Ⅱm RNA水平,改善哮喘小鼠气道重构。更多还原

【Abstract】 Objective To investigate the effectiveness of cysteinyl leukotriene receptor antagonist(montelukast,MK)on the pathological features and the transcription level of Arginase- Ⅱ in the asthmatic mice models. Methods Mice were randomly divided into the control,asthmatic, MK,and DXM groups. The thickness of the smooth muscle(WAm)of intrapulmonary bronchi was measured by image analysis system. The function of airway goblet cells was estimated by alcian blue staining. m RNA levels for arginase- Ⅱ were determined by RT-PCR. Results Obvious infiltration of inflammatory cells and proliferation of goblet cells and smooth muscle were demonstrated in mouse bronchus. Transcription levels of arginase- Ⅱ in the lung tissue were significantly higher than those of control group. Compared with asthmatic group,there was mild inflammation and collagen deposition in MKtreated and DXM-treated groups. Conclusion Repeated exposure of allergen induced airway inflammation and remodeling. Arginase- Ⅱ plays an important role in airway remodeling. MK and DXM intervention could inhibit airway remodeling through the way to reduce the levels of arginase- Ⅱ.更多还原