摘要
目的:观察Smad2/3和Smad7蛋白在大鼠哮喘血中性粒细胞(PMN)中的表达,探讨PMN能否通过Smads体系参与哮喘气道炎症的发病过程。方法:卵白蛋白(OVA)诱导大鼠哮喘模型,20只SD大鼠随机分成哮喘组和正常对照组,分离纯化血PMN,免疫细胞化学法检测PMN Smad2/3和Smad7蛋白的表达水平。结果:哮喘组(0.142±0.021,OD值)Smad2/3蛋白的表达水平显著高于正常对照组(0.081±0.011,OD值)(P<0.01),而哮喘组(0.125±0.024,OD值)Smad7蛋白的表达水平显著低于正常对照组(0.257±0.047,OD值)(P<0.01)。两者的表达呈显著负相关(n=19,r=-0.891,P<0.01)。结论:Smads体系在哮喘时处于失衡状态,受体调节型Smad占优势。哮喘时PMN合成Smad2/3和Smad7蛋白的功能增加,PMN可能部分通过Smads体系参与哮喘的气道炎症过程。
AIM： To observe the expressions of Sroad2/3 and Smad7 proteins at blood polymolphonuclear leukocyte （PMN） in rats asthma. And to determine whether PMN participate in airway inflammation of asthma via Sroads systenn. METHODS： Rat asthma model was induced by ovalbumin, twenty male Sprague-Danley rats were randomly divided into two groups on average, including asthma group and control group. Blood PMNs were isolated and purified. The expressions of Sroad2/3 and Sroad7 proteins were detected by immunocytochemical method at blood PMN. RESULTS： The expressions of Sroad2/3 protein were significantly higher in asthma group （0. 142 ± 0.021, optical density）than those in control group （0. 081 ± 0.011, optical density, P 〈 0.01）. But the expressions of Sroad7 protein were significantly lower in asth-ma group（0. 125 ±0.024, optical density） than those in control group（0.257 ± 0.047, optical density, P 〈 0.01）. There were significant statistical negtive correlation between the expression of Smad2/3 and Smad7 （n =19, r = - 0.891, P 〈 0.01）. CONCLUSION： Smads system is in imbalanced state in asthma exacerbation. Receptor-regnlated Smads is predomination. The synthesis function of PMN about Smad2/3 and Smad7 protein are increased in asthma exacerbation. PMN participated in airway inflammation of asthma may be via Smads systerm.
出处
《中国临床药理学与治疗学》
CAS
CSCD
2009年第4期405-409,共5页
Chinese Journal of Clinical Pharmacology and Therapeutics
基金
浙江省卫生厅基金资助项目(2007-B238)
温岭市科协基金资助项目(2006-27)
作者简介
童夏生，男，硕士，副主任医师，研究方向：儿科呼吸：Tel：13758688128.E-mail：xshtzg@163．com.
