布地奈德对支气管哮喘大鼠血中性粒细胞中转化生长因子β1及Smad2／3表达的影响

目的观察转化生长因子β1（transforrning growth factor beta-1，TGF-β1）及Smad2／3在支气管哮喘（简称哮喘）大鼠血中性粒细胞（polymorphonuclear leucocyte，PMN）中的表达及布地奈德对其的影响，探讨PMN通过TGF-β1／Smad信号通路参与哮喘气道炎症的可能作用机制。方法采用大鼠哮喘模型，随机分成哮喘组（A组）、正常对照组（C组）和布地奈德治疗组（B组），对血PMN进行分离纯化，免疫细胞化学法检测血PMN中TGF-β1和Smad2／3的表达水平。结果与C组（0．131±0．015OD值）相比，PMN TGF-β1的表达水平在A组（0．228±0．016OD值）和B组（0．164±0．01701）值）差异均具有统计学意义（P值均〈0．01）；B组与A组相比，TGF-β1的表达水平差异也具有统计学意义（P〈0．01）。与C组（0．081±0．011OD值）相比，PMN Smad2的表达水平在A组（0．142±0．021OD值）和B组（0．110±0．010OD值）差异均具有统计学意义（P值均〈0．01）；B组与A组相比，PMNSmad2／3的表达水平也具有显著统计学意义（P〈0．01）。两者的表达呈显著正相关（r=0．776，P〈0．01）。结论PMN能合成TGF—β1和Smad2／3，且哮喘时其合成水平增加，其合成功能可以被布地奈德所抑制。PMN可能通过TGF-β1／Smad信号转导途径参与哮喘的气道炎症讨程。

Effect of budesonide on expressions of transforming growth factor beta-1 and Smad2/3 at blood polymorphonuclear leucocyte in rat bronchial asthma model

Objective To observe the expression of transforming growth factor beta 1 （TGF-β1） and Smad2/3 at blood polymorpbonuclear leucocyte（PMN） and the effect of budesonide in rat bronchial asthma （asthma）. And to investigate whether PMN participates in airway inflammation of asthma via TGF-β1/Smad signal transduction pathway. Methods The rats model of asthma were randomly divided into three groups, including asthma group（group A）, control group（group C） and budesonide treated group （group B）. TGF-β1 and Smad2/3 were detected by immunocytochemical method at blood PMN. Results When compared with group C （0. 131 ±0. 015 optical density）, there were significant statistics of TGF-β1 expressions at blood PMN in group A （0. 228±0. 016 optical density） and in group B （0. 164±0. 017 optical density） （all P 〈0.01）. And there were significant statistics of TGF-β1 expressions between group A and group B （ P 〈0.01）. When compared with group C （0. 081± 0.011 optical density）, there were significant statistics of Smad2/3 expressions at blood PMN in group A （0. 142±0. 021 optical density） and in group B （0. 110±0. 010 optical density） （all P 〈0.01）. And there were significant statistics of Smad2/3 expressions between group A and group B（ P 〈0.01）. There were significantly positive correlations between the expressions of TGF-β1 and Smad2/3 （ r = 0. 776, P 〈 0.01）. Conclusions TGF-β1 and Smad2/3 can be synthesized by PMN,and their levels are increased in rats of asthma. But this function of PMN can be inhibitted by budesonide. Their expressions are positive correlated. PMN participates in airway inflammation of asthma possibly via TGF-β1/Smad signal transduction system.