Smad2／3和Smad7蛋白在血中性粒细胞中的表达与哮喘发病关系的实验性研究

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PMNSmad2／3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井目关（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Sinad2／3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。

Experimental study of the relationship between Smad2/3 and Smad7 proteins expressions in blood polymorphonuclear leucocyte and the asthma exacerbation

AIM: To observe the expressions of Smad2/3 and Smad7 proteins at blood polymorphonu-clear leukocyte (PMN) in rats asthma. And to determine whether PMN participate in airway inflammation of asthma via Smads system. 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 Smad2/3 and Smad7 proteins were detected by immunocytochemical method at blood PMN. RESULTS: The expressions of Smad2/3 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 Smad7 protein were significantly lower in asthma 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-regulated 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.