核因子κB与过氧化物酶体增殖物激活受体γ在类风湿性关节炎发病机制中的研究进展

Research progress of nuclear factor-κB and peroxisome proliferator-activated receptor-γ in the pathogenesis of rheumatoid arthritis

类风湿性关节炎(RA)是一种慢性、进行性、侵袭性、系统性、炎症性以累及周围关节为主的自身免疫病,特点是发病率高、致残率高。目前认为炎症反应是其发病的核心环节。在疾病过程中,炎症参与疾病每个阶段,导致血管异生进而血管翳增生、骨侵蚀和软骨破坏。过氧化物酶体增殖物激活受体γ(PPAR-γ)和核因子κB(NF-κB)抗炎、促炎机制的发现,PPAR-γ可通过抑制NF-κB途径诱导巨噬细胞的凋亡及NF-κB和PPAR-γ密切的关系为RA的研究提供了新的方向。本文针对PPAR-γ和NF-κB的情况作一综述。

Rheumatoid arthritis(RA) is a chronic, progressive, invasive, systematic and inflammatory autoimmune disease which mainly involves the surrounding joints. It is characterized by high incidence and high disability rate. At present, it is considered that inflammatory reaction is the core link of its pathogenesis. In the course of the disease, inflammation participates in every stage of the disease, leading to heterophysis and pannus proliferation, bone erosion and cartilage destruction. The discovery of anti-inflammatory and pro-inflammatory mechanisms of peroxisome proliferatoractivated receptor-γ(PPAR-γ) and nuclear factor-κB(NF-κB), the pathway that PPAR-γ can induce apoptosis of macrophages by inhibiting NF-κB, and the close relationship between NF-κB and PPAR-γ provides a new direction for the study of RA. In this paper, the situation of PPAR-γ and NF-κB is reviewed.