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类风湿关节炎中的氧化还原信号传导与炎症反应

Redox signalling and the inflammatory response in rheumatoid arthritis.

作者信息

Filippin L I, Vercelino R, Marroni N P, Xavier R M

机构信息

Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.

出版信息

Clin Exp Immunol. 2008 Jun;152(3):415-22. doi: 10.1111/j.1365-2249.2008.03634.x. Epub 2008 Apr 16.

Abstract

Reactive oxygen species (ROS) are produced mainly during oxidative phosphorylation and by activated phagocytic cells during oxidative burst. The excessive production of ROS can damage lipids, protein, membrane and nucleic acids. They also serve as important intracellular signalling that enhances the inflammatory response. Many studies have demonstrated a role of ROS in the pathogenesis of inflammatory chronic arthropathies, such as rheumatoid arthritis. It is known that ROS can function as a second messenger to activate nuclear factor kappa-B, which orchestrates the expression of a spectrum of genes involved in the inflammatory response. Therefore, an understanding of the complex interactions between these pathways might be useful for the development of novel therapeutic strategies for rheumatoid arthritis.

摘要

活性氧(ROS)主要在氧化磷酸化过程中产生,并在氧化爆发期间由活化的吞噬细胞产生。ROS的过量产生会损害脂质、蛋白质、膜和核酸。它们还作为重要的细胞内信号传导,增强炎症反应。许多研究已经证明ROS在炎症性慢性关节病(如类风湿性关节炎)的发病机制中起作用。已知ROS可以作为第二信使激活核因子κB,后者协调一系列参与炎症反应的基因的表达。因此,了解这些途径之间的复杂相互作用可能有助于开发类风湿性关节炎的新型治疗策略。

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