《生命科学》 2016, 28(3): 405-408
摘 要:摘 要: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。
Abstract: Abstract: Gout is a kind of inflammation caused by purine metabolism disturbance and deposits of monosodium urate (MSU) crystals. Nucleotide-binding oligomerization domain-like receptor protein 3 (NALP3) inflammasome is a protein complex which can be activated by MSU crystal when the crystal is swallowed by macrophage, then leading to gout inflammation reaction by cleaving caspase-1 to produce and release interleukin-1β. The activation and composition of NALP3 inflammasome, the identification of MSU crystal in the pathogenesis of gout, and the drugs targeting NALP3 inflammasome were summarized in this article.