促血管生成素-1及其受体Tie-2在哮喘大鼠气道中的表达  

Expression of angiopoietin-1 and its tyrosine kinase receptor Tie-2 in the airway of asthmatic rats

作　　者：乔俊英[1] 栾斌[1] 韩素鸽[2] 王秀芳[1] 

机构地区：[1]郑州大学第三附属医院儿内科,河南郑州450052 [2]郑州市妇幼保健院儿内科,河南郑州450052

出　　处：《中国当代儿科杂志》2008年第5期642-646,共5页Chinese Journal of Contemporary Pediatrics

摘　　要：目的通过建立哮喘大鼠模型,观察气道结构改变,探讨促血管生成素-1(Ang-1)及其受体(Tie-2)在哮喘大鼠气道中的表达和意义以及地塞米松对其的影响。方法Sprague-Dawley大鼠45只,随机分为对照组,模型组和地塞米松干预组。采用腹腔注射10%卵清蛋白致敏和1%卵清蛋白雾化吸入激发复制哮喘模型,干预组每次激发前给予地塞米松。采用免疫组化检测Ang-1及其受体Tie-2在不同组间气道壁表达变化;采用计算机病理图像分析系统分析各组气道壁厚度。结果①模型组气道壁厚度较对照组明显增加(33.9333±8.3791μm2/μmvs21.1333±2.7740μm2/μm,P<0.01),干预组为(27.4000±4.6105μm2/μm)较对照组增加(P<0.01),但较模型组明显减轻(P<0.01)。②模型组气道壁Ang-1及其受体Tie-2在气道上皮表达较对照组明显增加(103.9487±8.2914vs76.0320±3.7728,99.2307±8.1913vs75.3153±3.7321,P<0.01),干预组为(90.6180±5.2339,86.6633±3.7321)较对照组增加(P<0.01),但较模型组明显下降(P<0.01)。③直线相关分析显示气道壁Ang-1及其受体Tie-2的表达同气道壁厚度呈正相关,Ang-1与其受体Tie-2间也呈明显正相关,均P<0.01。结论哮喘模型大鼠气道壁中Ang-1及其受体Tie-2表达上调,并与气道壁厚度呈正相关,提示Ang-1及其受体Tie-2可能参与哮喘气道重建过程。地塞米松可下调Ang-1与其受体Tie-2在气道壁的表达,并可减轻气道结构改变。Objective To study the effect of dexamethasone on airway morphology and on the expression of angiopoietin-1 （Ang-1） and its tyrosine kinase receptor Tie-2 in the airway of asthmatic rats. Methods Forty-five Sprague-Dawley rats were randomly divided into control, asthmatic, and dexamethasone-treated asthmatic groups. Asthma was induced by repeated sensitization and challenge with ovalbumin in the latter two grouPs. The dexamethasone intervention group received an intraperitonea injection of dexamethasone （2 mg/kg） before asthma challenge. Immunohistochemistry was used to measure the expression of Ang-1 and Tie-2 in the airway, Airway thickness was estimated by a computerized digital image analyzer. Results Airway thickness in the asthmatic group （33. 9333 ± 8. 3791 μm^2/μm） increased significantly compared with that in the control group （ 21. 1333 ± 2. 7740 μm^2/μm ） （ P 〈 0.01 ）. The dexamethasone intervention group also showed increased thickness of the airway （27. 4000 ± 4. 6105 μm^2/μm） compared with the control group （P 〈 0.01 ）, but the airway thickness in the dexamethasone intervention group was significantly reduced compared with that in the untreated asthmatic group （P 〈 0.01 ）. The expression of Ang-1 （ 103. 9487 ± 8. 2914 vs 76.0320 ± 3.7728 ; P 〈 0.01） and Tie-2 （99. 2307 ± 8. 1913 vs 75. 3153 ± 3. 7321; P 〈 0.01 ） in the airway increased significantly in the asthmatic group compared to controls. The expression of Ang-1 and Tie-2 in the airway of the dexamethasone intervention group （90. 6180 ± 5. 2339 and 86. 6633 ± 3. 7321, respectively） was statistically higher than that in the control group （ P 〈 0.01 ） but statistically lower than that in the untreated asthmatic group （ P 〈 0.01 ）. Ang-1 and Tie-2 expression in the airway was positively correlated with the thickness of airway （ rAng-1 = 0.719, rTie-2 = 0. 746, P 〈 0.01 ）. There was also a positive correlation between Ang-1 and Tie-2 expression （r = 0. 742, P �

关 键 词：哮喘 气道重塑 促血管生成素-1 受体TIE-2 大鼠 

分 类 号：R562.25[医药卫生—呼吸系统]