| 摘要: |
| ［摘要］ 痛风是由于血尿酸浓度升高，尿酸钠晶体在关节、肌腱和周围组织中沉积，从而导致炎症性关节炎间歇性发作。Toll样受体是先天免疫系统中模式识别受体的一种。痛风性关节炎是由于过饱和的尿酸钠晶体在血液中析出，并与巨噬细胞产生作用，导致中性粒细胞的趋化、聚集，从而激活TLR2/TLR4-NF-κB信号通路，释放IL-1β、IL-6、TNF-α等炎性因子和蛋白酶，导致痛风性关节炎的发生、发展。该文以痛风及TLR2/TLR4-NF-κB信号通路为主线，综述了TLR2/TLR4-NF-κB信号通路与痛风的相关性以及以该信号通路为靶点的治疗方法。 |
| 关键词: 痛风 尿酸钠晶体 炎症 TLR2/TLR4-NF-κB信号通路 |
| DOI：10.3969/j.issn.1674-3806.2023.10.23 |
| 分类号:R 363.2+1 |
| 基金项目:西藏高原相关疾病分子机制与干预研究重点实验室开发项目（编号：KF2022002）；西藏民族大学医学院国家自然科学基金培育项目（编号：XZMU-M2022N03） |
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| Research progress of TLR2/TLR4-NF-κB signaling pathway in gout |
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BAI Dong-xue, LI Jing, MA Li-feng
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Key University Laboratory of Environment and Disease-Related Gene Research, Xizang Minzu University, Xianyang 712082, China
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| Abstract: |
| ［Abstract］ Gout is caused by the increase of blood uric acid concentration and the deposition of sodium urate crystals in joints, tendons and surrounding tissues,which leads to intermittent attacks of inflammatory joint disease. Toll-like receptor(TLR) is one of the pattern-recognition receptors(PRRs) in the innate immune system. It has been proved that gouty arthritis is caused by oversaturated monosodium urate(MSU) crystals precipitating in the blood and interacting with macrophages, which leads to the chemotaxis and aggregation of neutrophils, thus activating TLR2/TLR4-nuclear factor(NF)-κB signaling pathway and releasing inflammatory factors such as interleukin(IL)-1β, IL-6 and tumor necrosis factor-α(TNF-α), and proteases, leading to the occurrence and development of gouty arthritis. Taking gout and TLR2/TLR4-NF-κB signaling pathway as the main clue, this paper reviews the correlation between TLR2/TLR4-NF-κB signaling pathway and gout, and the treatment methods targeted by TLR2/TLR4-NF-κB signaling pathway. |
| Key words: Gout Monosodium urate crystals Inflammation TLR2/TLR4-NF-κB signaling pathway |
