小窝蛋白1介导TGF-β信号通道调控肺细胞外基质重塑机制研究  

The Research of Caveolin1 to Regulate Lung Extracellular Matrix Remodeling by Mediating TGF-β Signal Pathway

作　　者：周游[1] 孙伏喜[1] 周蓉[1] 牛常明[1] 郭骏华[1] 

机构地区：[1]南京医科大学第二附属医院,江苏南京210011

出　　处：《中国医学创新》2014年第23期16-20,共5页Medical Innovation of China

摘　　要：目的:探讨caveolin-1通过介导TGF-β信号通道在体外调控小鼠肺细胞外基质重塑的机制研究。方法:选取cav1-/-小鼠作为动物模型设为实验组,野生型C57BL/6J小鼠设为对照组,检测肺机械性指标,测定Ⅰ型胶原纤维与弹性纤维含量及mRNA水平,检测肺血管蛋白渗出及支气管灌洗液(BAL)中细胞含量及细胞因子水平,测定TGF-β下游信号分子Smad2及ERK1/2水平。结果:与对照组比较,实验组中肺顺应性下降,僵硬度增加(P<0.05);BAL中总蛋白及白蛋白水平和静脉注射伊文思蓝在肺组织的含量均明显增加(P<0.05);Ⅰ型胶原纤维与弹性纤维含量及mRNA水平增加(P<0.05);Smad2及ERK1/2水平均明显提高(P<0.05);但BAL中细胞含量及细胞因子水平无差异。结论:小窝蛋白1通过介导TGF-β信号转导在体外上调细胞外基质重塑,促进肺纤维化发生。Objective：To investigate the research of caveolin1 to regulate lung extracellular matrix remodeling by mediating TGF-βsignal pathway.Method：C57BL/6J cav1-/-mice were selected as experimental group,and C57BL/6J wild type mice were determined as control group.Lung mechanics index of all mice were measured,typeⅠcollagenous fibrils and elastic fiber deposition and mRNA level were assayed,lung vascular leakage and cell content＆amp;cytokines level in bronchoalveolar lavage were measured,Smad2 and ERK1/2 level regarding as TGF-βdownstream signaling molecule were evaluated.Result：Compared with the control group,the lung compliance was down-regulated,elastance and airway resistance were up-regulated in the experimental group（P〈0.05）.The total protein and albumin levels in BAL and intravenous injection of Evans blue content in lung tissue were significantly increased in experimental group（P〈0.05）. The expression of typeⅠcollagenous fibrils and elastic fiber deposition and mRNA level were increased in experimental group（P〈0.05）.Smad2 and ERK1/2 level were significantly improved（P〈0.05）,but cell content and cytokines level in BAL were no significant deviation.Conclusion：Caveolin1 can up-regulate lung extracellular matrix remodeling by mediating TGF-βsignal pathway in vitro and progress pulmonary fibrosis.

关 键 词：小窝蛋白1 TGF-Β 细胞外基质 信号传导 肺纤维化 

分 类 号：R563.8[医药卫生—呼吸系统]