Lipid Peroxidation-Mediated Inflammation Promotes Cell Apoptosis through Activation of NF-κB Pathway in Rheumatoid Arthritis Synovial CellsReportar como inadecuado




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Mediators of Inflammation - Volume 2015 2015, Article ID 460310, 10 pages -

Research ArticleDepartment of Rheumatology and Immunology, West China Hospital of Sichuan University, Chengdu, Sichuan 610041, China

Received 15 November 2014; Revised 23 January 2015; Accepted 23 January 2015

Academic Editor: Helen C. Steel

Copyright © 2015 Geng Yin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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.





Autor: Geng Yin, Ying Wang, Xiao-min Cen, Min Yang, Yan Liang, and Qi-bing Xie

Fuente: https://www.hindawi.com/



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