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哮喘气道重塑大鼠中磷酸化p38丝裂原活化蛋白激酶的表达对黏液细胞增殖的影响及布地奈德的干预作用
引用本文:郑仰明,李昌崇,张维溪,管小俊.哮喘气道重塑大鼠中磷酸化p38丝裂原活化蛋白激酶的表达对黏液细胞增殖的影响及布地奈德的干预作用[J].中国临床药理学与治疗学,2009,14(8):866-871.
作者姓名:郑仰明  李昌崇  张维溪  管小俊
作者单位:温州医学院附属育英儿童医院呼吸科,温州,325027,浙江
摘    要:目的:观察磷酸化p38丝裂原活化蛋白激酶在哮喘气道重塑大鼠肺组织的表达及对其黏液细胞增殖的作用及布地奈德对哮喘气道重塑大鼠肺组织中磷酸化p38丝裂原活化蛋白激酶的表达和黏液细胞增殖的干预作用。方法:30只雄性SD大鼠随机分为对照组(C组)、哮喘气道重塑组(A组)、布地奈德治疗组(B组)。建立哮喘气道重塑模型,肺组织用于Masson三色染色、过碘酸.雪夫氏染色,免疫组化染色,光镜电镜观察。结果:光镜及电镜均发现A组明显的气道重塑病理改变,B组较A组有所减轻;图像分析结果:支气管壁厚度及平滑肌厚度比较,A组均明显高于C组,B组明显低于A组,但仍高于C组。气道黏液细胞百分比比较,A组明显高于C组(P〈0.01),B组明显低于A组(P〈0.05),但B组仍高于C组(P〈0.01)。各组大鼠气道上皮磷酸化p38MAPK表达的比较,A组明显高于C组(P〈0.01);B组明显低于A组(P〈0.05)。磷酸化p38MAPK表达水平与黏液细胞百分比呈显著正相关(n=30,r=0.813,P〈0.01)。结论:气道上皮磷酸化p38MAPK表达增加可能促使哮喘气道重塑大鼠黏液细胞增殖;布地奈德能抑制哮喘气道重塑大鼠中磷酸化p38MAPK的表达从而抑制黏液细胞增殖。

关 键 词:哮喘  大鼠  气道重塑  黏液细胞  布地奈德

Expression of phospho-p38MAPK in asthmatic rats with airway remodeling the effect on proliferation of mucous cells and the regulation of budesonide
ZHENG Yang-ming,LI Chang-chong,Zhang Wei-xi,GUAN Xiao-jun.Expression of phospho-p38MAPK in asthmatic rats with airway remodeling the effect on proliferation of mucous cells and the regulation of budesonide[J].Chinese Journal of Clinical Pharmacology and Therapeutics,2009,14(8):866-871.
Authors:ZHENG Yang-ming  LI Chang-chong  Zhang Wei-xi  GUAN Xiao-jun
Institution:( Department of Respiratory Medicine,Yuying Children's Hospital Affiliated to Wenzhou Medical College,Wenzhou 325027,Zhejiang,China)
Abstract:AIM:To investigate the protein expression of phospho-p38MAPK in asthmatic rats with airway remodeling and its effects on proliferation of mucous cells and the regulation role of budesonide.METHODS:Thirty male rats were randomly divided into control group(Group C,n=10),airway remodeling group(Group A,n=10) and budesonide treated group(Group B,n=10).The asthmatic rat model with airway remodeling was established.The lung tissue was observed by Hematoxylin and eosin staining,Masson's Trichrome stain,Periodic Acide Schiff' and immunohistochemistry staining.RESULTS:Pathological changes of airway remodeling were found under light microscope and TEM.Compared with Group A,the pathologic change in group B was relieved.The results of image analysis:compared with Group A,the total bronchial wall area(Wat) and the smooth muscle area (Wam) and the percentage of mucous cells in rat airway epithelium were significantly decreased in Group C and Group B,but the Wat and Wam in group B were higher than those in Group C.Compared with Group A,the contents of phospho-p38MAPK protein in group B and group C were decreased.There were significant positive correlation between the contents of phosphop38MAPK and percentage of mucous cells(n=30,r =0.813,P<0.01).CONCLUSION:High expression of phospho-p38MAPK might precipitate the proliferation of mucous cells in asthmatic rats.Budesonide can inhibit the expression of phospho-p38MAPK protein in the airway epithelium of asthmatic rats with airway remodeling,by which might inhibit proliferation of mucous cells.
Keywords:asthma  rat  airway remodeling  mucous cell  budesonide
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