CAJ | 학술논문

目的观察转化生长因子β1(transforming 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-B1和Smad2/3的表达水平.结果与C组(0.131±0.015 OD值)相比,PMN TGF-β1的表达水平在A组(0.228±0.016 OD值)和B组(0.164±0.017 OD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±0.011 OD值)相比,PMN Smad2的表达水平在A组(0.142±0.021 OD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,PMN Smad2/3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-β/Smad信号转导途径参与哮喘的气道炎症过程.
목적 관찰전화생장인자β1(transforming growth factor beta-1,TGF-β1)급Smad2/3재지기관효천(간칭효천)대서혈중성립세포(polymorphonuclear leucocyte,PMN)중적표체급포지내덕대기적영향,탐토PMN통과TGF-β1/Smad신호통로삼여효천기도염증적가능작용궤제.방법 채용대서효천모형,수궤분성효천조(A조)、정상대조조(C조)화포지내덕치료조(B조),대혈PMN진행분리순화,면역세포화학법검측혈PMN중TGF-B1화Smad2/3적표체수평.결과 여C조(0.131±0.015 OD치)상비,PMN TGF-β1적표체수평재A조(0.228±0.016 OD치)화B조(0.164±0.017 OD치)차이균구유통계학의의(P치균＜0.01);B조여A조상비,TGF-β1적표체수평차이야구유통계학의의(P＜0.01).여C조(0.081±0.011 OD치)상비,PMN Smad2적표체수평재A조(0.142±0.021 OD치)화B조(0.110±0.010OD치)차이균구유통계학의의(P치균＜0.01);B조여A조상비,PMN Smad2/3적표체수평야구유현저통계학의의(P＜0.01).량자적표체정현저정상관(r=0.776,P＜0.01).결론 PMN능합성TGF-β1화Smad2/3,차효천시기합성수평증가,기합성공능가이피포지내덕소억제.PMN가능통과TGF-β/Smad신호전도도경삼여효천적기도염증과정.
Objective To observe the expression of transforming growth factor beta-1(TGF-β1) and Smad2/3 at blood polymorphonuclear 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.