Abstract:
:Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic inflammation of multiple joints. The central pathogenesis of RA is the proliferation of synovial fibroblasts in response to inflammatory cytokines. However, some of the targeted therapies for inflammation reactions do not display significant clinical improvement after initiation of therapy. Thus, the relationship between inflammatory responses and RA therapy is still incompletely understood. In the present study, we proposed to determine whether enhanced inflammations may lead to cell apoptosis in rheumatoid arthritis synoviocytes. Our results indicated that products of lipid peroxidations, 4-HNE, may induce synovial intrinsic inflammations by activating NF-κB pathways and it may lead to cell apoptosis. Pharmacological inhibition of NF-κB activation may reduce the 4-HNE mediated inflammation responses and subsequent cell apoptosis. Our results may help to clarify the role of inflammations on RA development and imply that blocking NF-κB activation may be partly beneficial for human RA therapy. These findings might provide a mechanism-based rationale for developing new strategy to RA clinical therapy.
journal_name
Mediators Inflammjournal_title
Mediators of inflammationauthors
Yin G,Wang Y,Cen XM,Yang M,Liang Y,Xie QBdoi
10.1155/2015/460310subject
Has Abstractpub_date
2015-01-01 00:00:00pages
460310eissn
0962-9351issn
1466-1861journal_volume
2015pub_type
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journal_title:Mediators of inflammation
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更新日期:2019-11-03 00:00:00
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journal_title:Mediators of inflammation
pub_type: 杂志文章,评审
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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doi:10.1080/09629350310001599639
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journal_title:Mediators of inflammation
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abstract:STUDY OBJECTIVES:To assess serum amyloid alpha (SAA) pleural fluid levels in parapneumonic effusion (PPE) and to investigate SAA diagnostic performance in PPE diagnosis and outcome. METHODS:We studied prospectively 57 consecutive patients with PPE (empyema (EMP), complicated (CPE), and uncomplicated parapneumonic effu...
journal_title:Mediators of inflammation
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doi:10.1155/2011/237638
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
pub_type: 杂志文章
doi:10.1155/2016/1232103
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journal_title:Mediators of inflammation
pub_type: 杂志文章,评审
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journal_title:Mediators of inflammation
pub_type: 杂志文章,评审
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journal_title:Mediators of inflammation
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doi:10.1080/09629350400014099
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journal_title:Mediators of inflammation
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doi:10.1155/2018/6039171
更新日期:2018-03-08 00:00:00
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journal_title:Mediators of inflammation
pub_type: 杂志文章
doi:10.1155/S0962935193000444
更新日期:1993-01-01 00:00:00
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journal_title:Mediators of inflammation
pub_type: 杂志文章
doi:10.1155/MI/2006/12919
更新日期:2006-01-01 00:00:00
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journal_title:Mediators of inflammation
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doi:10.1155/S0962935195000032
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
pub_type: 杂志文章
doi:10.1155/2013/461536
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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doi:10.1155/2014/386148
更新日期:2014-01-01 00:00:00
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journal_title:Mediators of inflammation
pub_type: 杂志文章,评审
doi:10.1155/2010/413238
更新日期:2010-01-01 00:00:00
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journal_title:Mediators of inflammation
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doi:10.1155/S0962935194000499
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journal_title:Mediators of inflammation
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doi:10.1155/2009/850940
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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