痛风是体内嘌呤代谢紊乱引起尿酸钠盐沉积所致的晶体相关性疾病。近年研究表明,核苷酸结合寡聚化结构域样受体3(nucleotide-binding oligomerization domain-like receptor protein 3,NALP3)炎性体活化与巨噬细胞吞噬尿酸钠晶体密切相关。NALP3炎性体活化后可剪切半胱天冬酶-1并促进白介素1β释放,引起痛风炎症反应。现将从NALP3炎性体的组成及活化、尿酸钠晶体的吞噬识别途径,以及以NALP3炎性体为靶点的抗痛风药物等方面作一综述。 Gout is a crystal-related disease caused by uric acid sodium salt deposition in the purine metabolic disorder in the body. Recent studies show that activation of nucleotide-binding oligomerization domain-like receptor protein 3 (NALP3) inflammasome is closely related to macrophage phagocytosis of sodium urate crystals. Activation of the NALP3 inflammasome cleaves caspase-1 and promotes the release of interleukin-1β, causing gout inflammation. Now we will review the composition and activation of NALP3 inflammasome, the phagocytic recognition pathway of sodium urate crystals and the anti-gout drugs targeting NALP3 inflammasome.