TDI通过PI3K通路下调气道上皮粘附连接分子β-catenin的表达

来源 :中华医学会2014年全国变态反应学术会议 | 被引量 : 0次 | 上传用户:z7228279
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目的 甲苯二异氰酸酯(TDI)是最常见的职业性哮喘的致病因素之一,TDI哮喘约占成年人哮喘的9%-15%.TDI哮喘具有与过敏性哮喘相似的临床特征,但其确切机制尚有待于进一步阐明.我们前期已经在体内外证明TDI可以引起气道上皮细胞屏障功能破坏,本研究进一步探讨TDI对哮喘气道上皮粘附连接分子破坏的分子机制.方法 按既往建立的方法建立TDI哮喘模型.评价LY294002处理后对气道炎症,气道反应性及粘附连接分子的影响.
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