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作 者:童夏生[1] 罗冬娇[2] 方慧英 方丽 王恩智[1] 陈豪[1] 叶辉[5]
机构地区:[1]台州中西医结合医院 [2]杭州师范大学钱江学院医学系 [3]诸暨市妇幼医院儿科 [4]诸暨市人民医院儿科 [5]台州市第一医院
出 处:《中国临床药理学与治疗学》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)
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.
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