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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Sma(12/3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 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.