目的观察气道高反应过程中黏附分子相关蛋白a1(catenin phaJjke1,cTNNAL1)的表达与呼吸道阻力的相关性。方法:取30只无特定病原体级Wister大鼠随机分为s组:正常对照组,臭氧攻击2d组,臭氧攻击4d组,臭氧攻击6d组,臭氧攻击6d+地塞米松治疗2d组;每组6只。原位杂交定位CTNNAL1的分布及表达,荧光定量RT-PCR检测CTNNAL1表达,Buxco动物肺功能分析系统检测呼吸道阻力,分析CTNNAL1表达和气道高反应时呼吸道阻力变化的相关陛。结果:在支气管上皮细胞、杯状细胞、血管内皮细胞及肺泡壁都分布有CTNNAL1。随着臭氧攻击的时间延长,CTNNAL1mRNA表达逐渐下调,气道高反应的程度加重,气道阻力逐渐增加。结论:在气道高反应过程中CTNNAL1mRNA表达下调,呼吸道阻力加重。CTNNAL1mRNA的表达与呼吸道阻力呈负相关。CTNNAL1是一种与气道高反应易感I生有关的黏附分子。
Objective: To observe the relation between in rats with airway hyperresponsiveness. the expression of CTNNAL1 and the airway resistance Methods: Thirty Wister rats were randomly divided into 5 groups: a normal control group, a 2 d ozone attack group, a 4 d ozone attack group, a 6 d ozone attack group, and a 6 d ozone attack+2 d dexamethasone treatment group (6 rats in each group). The distribution of CTNNAL1 was observed by in situ hybridization; the expression of CTNNAL1 was detected by fluorescence quantitative RT-PCR; the airway resistance was detected in by Buxco pulmonary function analysis system; and the relevance of the expression of CTNNAL1 and the resistance of respiratory tract in rat with airway hyperresponsiveness were analyzed. Results: CTNNAL1 was distributed in bronchial epithelial cells, goblet cells, endothelial cells, andthe alveolar wall. With the increase of the ozone attack, the expression of CTNNAL1 mRNA gradually reduced, the airway hyperresponsiveness was aggravated, and the airway resistance was increased. Conclusion: During airway hyperresponse, the reduction of CTNNAL1 mRNA can increase the airway resistance. There is a negative correlation between the reduction of CTNNAL1 mRNA and the airway hyperresponsiveness. CTNNAL1 is an adhesion molecule related to airway hyperresponsiveness susceptibility.