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。
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.
出处
《生命科学》
CSCD
2016年第3期405-408,共4页
Chinese Bulletin of Life Sciences
基金
国家自然科学基金项目(81573670)
