论文部分内容阅读
目的 研究纤维连接蛋白 (FN)在肺纤维化中的作用。方法 用免疫组织化学方法观察实验性大鼠肺纤维化纤维连接蛋白 (FN)的动态变化 ;用Northern印迹杂交和免疫细胞化学方法分别观察FN对体外培养的大鼠肺成纤维细胞Ⅰ、Ⅲ型前胶原mRNA和蛋白表达的影响。结果 (1)实验性肺纤维化大鼠肺组织内FN的含量持续增多 ;(2 )体外培养的肺成纤维细胞经FN作用 2h ,Ⅰ、Ⅲ型前胶原mRNA的表达即增强 ,分别在 12h、6h达到最大值 ,平均吸光度 (A值 )为对照组的 1 7、3 2倍 ;Ⅰ、Ⅲ型前胶原蛋白的表达亦增强 (P <0 0 1)。抗FN受体的抗体能部分抑制FN对胶原表达的上调作用 (P <0 0 5 )。结论 FN能够促进大鼠肺成纤维细胞合成Ⅰ、Ⅲ型胶原 ,其调控机制之一是在转录水平上增强了前胶原mRNA的表达
Objective To investigate the role of fibronectin (FN) in pulmonary fibrosis. Methods The dynamic changes of fibronectin (FN) in experimental rats were observed by immunohistochemical method. The expressions of fibronectin (FN) and fibronectin (FN) in rat lung fibroblasts were detected by Northern blotting and immunocytochemistry respectively. Effect of procollagen mRNA and protein expression. Results (1) The content of FN in lung tissue of rats with experimental pulmonary fibrosis continued to increase. (2) The expression of procollagen mRNA of type Ⅰ and type Ⅲ in lung fibroblasts cultured in vitro increased by FN for 2 hours, , Reached the maximum at 6h, and the average absorbance (A value) was 17.32 times that of the control group. The expressions of type Ⅰ and Ⅲ procollagen also increased (P <0.01). Anti-FN receptor antibodies partially inhibited the up-regulation of collagen expression by FN (P <0 05). Conclusions FN can promote the synthesis of type Ⅰ and type Ⅲ collagen in rat lung fibroblasts. One of the regulatory mechanisms is that the expression of procollagen mRNA is enhanced at the transcriptional level