罗格列酮对哮喘小鼠气道黏液高分泌的影响

Influence of rosiglitazone on mucus hypersecretion in asthmatic mice airway

目的:探讨过氧化物酶体增殖物激活受体-γ激动剂罗格列酮对哮喘小鼠气道黏液高分泌的影响及可能机制。方法:小鼠随机分为正常对照组、哮喘组和罗格列酮干预组,分别用RT-PCR法和免疫组织化学法测定小鼠肺组织T-betmRNA和气道黏蛋白Muc5ac蛋白的表达。结果:(1)哮喘组肺组织T-betmRNA的表达明显低于对照组(P<0.01),而哮喘组气道Muc5ac蛋白的表达显著高于对照组(P<0.01)。(2)罗格列酮组小鼠肺组织T-betmRNA的表达明显高于哮喘组(P<0.01),而罗格列酮组气道Muc5ac蛋白的表达则显著低于哮喘组(P<0.01)。(3)哮喘组T-betmRNA与Muc5ac蛋白呈线性负相关(P<0.05)。结论:罗格列酮能抑制哮喘时气道Muc5ac蛋白的表达,可能与其上调T-betmRNA的表达有关。

Objective To investigate the influence of rosiglitazone, an agonist of peroxisome proliferatirs activated receptor gamma （PPAR-γ）, on mucus hypersecretion in asthmatic mice airway and it＇s possible mechanisms. Methods Mice were randomized into three groups： control group, asthma model group and rosiglitazone group. Expression of T-bet mRNA in lung and Muc5ac protein in airway were detected by reverse transcription-polymerase chain reaction （RT-PCR） and immuno-histoehemical assay （ICH） technique respectively in three groups. Results （1）T-bet mRNA expression in lung of asthma model group decreased more obviously than that of control group （P 〈 0.01 ）. The expression of Muc5ac protein in airway of asthma model group was significantly higher than that of control group （P 〈 0.01）. （2）T-bet mRNA expression in Lung of rosiglitazone group elevated more obviously than that of asthma model group （P 〈 0.01 ）. Muc5ae protein expression in airway of rosiglitazone group decreased significantly than that of asthma model group （P 〈 0.01 ）. （3）There was significant negative relationship between the expression of T-bet mRNA in lung and MucSac protein in airway of asthma model group （P 〈 0.05）. Conclusion Rosiglitazone can suppress mucus overprodution and may cause these changes through altering the expression of T-bet mRNA.