IR@PKUHSC  > 北京大学第一临床医学院  > 儿科
学科主题临床医学
L-cystathionine inhibits oxidized low density lipoprotein-induced THP-1-derived macrophage inflammatory cytokine monocyte chemoattractant protein-1 generation via the NF-kappa B pathway
Zhu, Mingzhu1; Du, Junbao1,2,3; Liu, Angie Dong4; Holmberg, Lukas4; Chen, Selena Y.5; Bu, Dingfang6; Tang, Chaoshu2,7; Jin, Hongfang1
刊名SCIENTIFIC REPORTS
2015-05-28
DOI10.1038/srep10453
5
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Multidisciplinary Sciences
研究领域[WOS]Science & Technology - Other Topics
关键词[WOS]HYDROGEN-SULFIDE ; ATHEROSCLEROSIS ; CELLS ; EXPRESSION ; GENE ; NEUTROPHILS ; METABOLISM ; APOPTOSIS ; PROTECTS ; KETIMINE
英文摘要

This study aimed to explore whether and how L-cystathionine had any regulatory effect on the inflammatory response in THP-1-derived macrophages cultured in vitro under oxidized low-density lipoprotein (ox-LDL) stimulation. The human monocyte line THP-1 cell was cultured in vitro and differentiated into macrophages after 24 hours of PMA induction. Macrophages were pretreated with L-cystathionine and then treated with ox-LDL. The results showed that compared with the controls, ox-LDL stimulation significantly upregulated the expression of THP-1-derived macrophage MCP-1 by enhancing NF-kappa B p65 phosphorylation, nuclear translocation and DNA binding with the MCP-1 promoter. Compared with the ox-LDL group, 0.3 mmol/L and 1.0 mmol/L L-cystathionine significantly inhibited the expression of THP-1-derived macrophage MCP-1. Mechanistically, 0.3 mmol/L and 1.0 mmol/L L-cystathionine suppressed phosphorylation and nuclear translocation of the NF-kappa B p65 protein, as well as the DNA binding activity and DNA binding level of NF-kappa B with the MCP-1 promoter, which resulted in a reduced THP-1-derived macrophage MCP-1 generation. This study suggests that L-cystathionine could inhibit the expression of MCP-1 in THP-1-derived macrophages induced by ox-LDL via inhibition of NF-kappa B p65 phosphorylation, nuclear translocation, and binding of the MCP-1 promoter sequence after entry into the nucleus.

语种英语
WOS记录号WOS:000355546600001
项目编号31130030 ; 81370154 ; 91439110 ; 2012CB517806 ; 2011CB503904 ; NCET-11-0005
资助机构National Natural Science Foundation of China ; Major Basic Research Project of China ; Program for New Century Excellent Talents of Ministry of Education, China
引用统计
被引频次:5[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/52783
专题北京大学第一临床医学院_儿科
作者单位1.Peking Univ, Hosp 1, Cent Lab, Beijing 100034, Peoples R China
2.Peking Univ, Hosp 1, Dept Pediat, Beijing 100034, Peoples R China
3.Minist Educ, Key Lab Mol Cardiol, Beijing 100191, Peoples R China
4.Linkoping Univ, Dept Med & Hlth Sci, S-58183 Linkoping, Sweden
5.Univ Calif San Diego, La Jolla, CA 92093 USA
6.Peking Univ, Hlth Sci Ctr, Ctr Mol & Translat Med, Beijing 100191, Peoples R China
7.Peking Univ, Hlth Sci Ctr, Dept Physiol & Pathophysiol, Beijing 100191, Peoples R China
推荐引用方式
GB/T 7714
Zhu, Mingzhu,Du, Junbao,Liu, Angie Dong,et al. L-cystathionine inhibits oxidized low density lipoprotein-induced THP-1-derived macrophage inflammatory cytokine monocyte chemoattractant protein-1 generation via the NF-kappa B pathway[J]. SCIENTIFIC REPORTS,2015,5.
APA Zhu, Mingzhu.,Du, Junbao.,Liu, Angie Dong.,Holmberg, Lukas.,Chen, Selena Y..,...&Jin, Hongfang.(2015).L-cystathionine inhibits oxidized low density lipoprotein-induced THP-1-derived macrophage inflammatory cytokine monocyte chemoattractant protein-1 generation via the NF-kappa B pathway.SCIENTIFIC REPORTS,5.
MLA Zhu, Mingzhu,et al."L-cystathionine inhibits oxidized low density lipoprotein-induced THP-1-derived macrophage inflammatory cytokine monocyte chemoattractant protein-1 generation via the NF-kappa B pathway".SCIENTIFIC REPORTS 5(2015).
条目包含的文件
条目无相关文件。
个性服务
推荐该条目
保存到收藏夹
查看访问统计
导出为Endnote文件
谷歌学术
谷歌学术中相似的文章
[Zhu, Mingzhu]的文章
[Du, Junbao]的文章
[Liu, Angie Dong]的文章
百度学术
百度学术中相似的文章
[Zhu, Mingzhu]的文章
[Du, Junbao]的文章
[Liu, Angie Dong]的文章
必应学术
必应学术中相似的文章
[Zhu, Mingzhu]的文章
[Du, Junbao]的文章
[Liu, Angie Dong]的文章
相关权益政策
暂无数据
收藏/分享
所有评论 (0)
暂无评论
 

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。