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COPD大鼠原代肺动脉平滑肌细胞中MCP-1、TGF-β1和TLR4蛋白的检测
  • ISSN号:1671-6825
  • 期刊名称:《郑州大学学报:医学版》
  • 时间:0
  • 分类:R563.3[医药卫生—呼吸系统;医药卫生—临床医学;医药卫生—内科学]
  • 作者机构:桂林医学院附属医院呼吸内科,广西桂林541001
  • 相关基金:国家自然科学基金资助项目81360010; 广西省卫生厅自然科学基金资助项目S201603
中文摘要:

目的:探讨慢性阻塞性肺疾病(COPD)大鼠远端原代肺动脉平滑肌细胞(PASMCs)中单核细胞趋化蛋白-1(MCP-1)、转化生长因子-β1(TGF-β1)的分泌情况及其与Toll样受体4(TLR4)信号通路的相关性。方法:通过脂多糖(LPS)诱导建立大鼠COPD模型,分离培养、鉴定原代大鼠PASMCs,以LPS诱导PASMCs,然后分组(对照组、LPS组、TAK-242组,LPS+TAK-242组)培养细胞,用Western blot法检测各组PASMCs中TLR4的表达,ELISA法检测细胞培养上清液MCP-1、TGF-β1的浓度,并进行相关性分析。结果:LPS组较对照组PASMCs中TLR4的表达水平上调(P〈0.05),细胞培养上清液中MCP-1、TGF-β1的含量升高(P〈0.05);TAK-242组PASMCs中TLR4的表达水平下调(P〈0.05),上清液中MCP-1、TGF-β1与TLR4无相关性。结论:LPS可诱导大鼠原代PASMCs合成分泌MCP-1、TGF-β1,同时上调TLR4表达水平。

英文摘要:

Aim: To probe into the secretion of monocyte chemoattractant protein 1( MCP-1),transforming growth factor β1( TGF-β1) in primary pulmonary artery smooth muscle cells( PASMCs) of chronic obstructive pulmonary disease( COPD) rats and the correlation with toll-like receptor 4( TLR4) signaling pathways. Methods: The COPD rat model was established,and the PASMCs were separated,induced by LPS,and then divided into control group,LPS group,TAK-242 group,and LPS + TAK-242 group. The expression of TLR4 in PASMCs of each group was detected by Western blot,and the concentrations of MCP-1 and TGF-β1 in cell culture fluid were determined by ELISA,and at last a correlation analysis was conducted. Results: In contrast with the control group,the expression of TLR4 in PASMCs of the LPS group was inecreased( P〈0. 05) and the concentrations of MCP-1 and TGF-β1 in cell culture fluid were increased( P〈0. 05). The expression of TLR4 in PASMCs of the TAK-242 group was down-regulated( P〈0. 05) and the concentrations of MCP-1 and TGF-β1 in cell culture fluid showed no correlation with the expression of TLR4. Conclusion: LPS can induce PASMCs of rats to synthesize and secrete MCP-1 and TGF-β1,and the TLR4 is up-expressed at the same time.

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期刊信息
  • 《郑州大学学报:医学版》
  • 中国科技核心期刊
  • 主管单位:河南省教育厅
  • 主办单位:郑州大学
  • 主编:辛世俊
  • 地址:郑州市高新区科学大道100号
  • 邮编:450001
  • 邮箱:xzshi@126.com
  • 电话:0371-67781728
  • 国际标准刊号:ISSN:1671-6825
  • 国内统一刊号:ISSN:41-1340/R
  • 邮发代号:36-111
  • 获奖情况:
  • 综合性医药卫生类核心期刊,教育部优秀科技期刊一等奖,中国优秀科技期刊二等奖
  • 国内外数据库收录:
  • 美国化学文摘(网络版),波兰哥白尼索引,美国剑桥科学文摘,中国中国科技核心期刊,中国北大核心期刊(2008版),中国北大核心期刊(2011版),中国北大核心期刊(2014版)
  • 被引量:15607