欢迎您！东篱公司
退出
-
申报数据库
-
立项数据库
-
成果数据库
-
项目获奖数据库
中文摘要：
目的：探讨TLR-4信号通路在COPD大鼠肺动脉平滑肌细胞合成分泌IFN-γ、PDGF-AB中的作用。方法：消化、分离及纯化COPD大鼠原代肺动脉平滑肌细胞（PASMCs）,并随机分为：对照组、LPS组、TLR-4抑制剂组（TAK242）、LPS＋TAK242组;RT-PCR、Western blot法检测各组PASMCs中TLR4和NF-κB的基因表达水平;ELISA法检测PASMCs上清液中IFN-γ、PDGF-AB的水平。结果：与对照组比较,LPS组TLR-4和NF-κB的基因表达水平及上清液中IFN-γ、PDGF-AB的表达水平显著升高（P〈0.05）,而TAK242组显著降低（P〈0.05）;使用TAK242预处理后,再给予相同浓度LPS刺激,与LPS组相比,其表达水平显著下降（P〈0.05）。结论 ：LPS介导的TLR4信号通路参与COPD大鼠PASMCs合成分泌IFN-γ、PDGF-AB因子的调控,进而影响炎症反应及肺血管重塑。本实验为临床早期干预COPD提供了理论依据。
英文摘要：
Objective To study the function of the toll-like receptor-4（TLR-4） signaling pathway in the synthesis and secretion of pulmonary artery smooth muscle cells of rats with COPD. Methods The primary pulmonary artery smooth muscle cells（PASMCs） of rats with COPD were digested, separated and purified. Then they were randomly divided into control group, LPS group, TLR4 inhibitor group（TAK242） and LPS ＋ TLR4 inhibitor group. RT-PCR, Western blot were used to detect the expression level of TLR-4 and NF-κB among groups. The levels of IFN-γ and PDGF-AB in supernatant with PASMCs in each group were detected by ELISA.Results LPS increased the expression of TLR-4、 NF-κB and the levels of IFN-γ and PDGF-AB. The expression of TLR4, NF-κB and the levels of IFN-γ and PDGF-AB were significantly reduced after inhibiting the expression of TLR4（P〈0.05）. Conclusion TLR-4 signaling pathway involved in the inflammatory response and pulmonary vascular remodeling which increased the synthesis and secretion of IFN-γ and PDGF-AB in PASMCs. It provides a theoretical approach for the early intervention of clinical with COPD.
同期刊论文项目
同项目期刊论文
期刊信息
位置：