目前我国痛风患病率高达2.2%，接近西方发达国家水平。最新资料显示，TLR/MyD88/NF-κB通路与NLRP3/ASC/caspase-1轴协同激活IL-1β，在尿酸钠晶体（MSU）诱导的痛风性关节炎（GA）中发挥关键作用，这为痛风治疗药物的研制带来了新的契机。我们前期研究发现土茯苓总黄酮（TFSG）具有良好的抗大鼠GA功效，并能显著抑制MSU刺激的小鼠骨髓来源巨噬细胞（BMDMs）中IL-1β产生及NLRP3炎性体表达。本项目拟以GA大鼠和单核巨噬细胞（THP-1）为对象，借助现代分子生物学技术，结合流式细胞术、激光共聚焦等手段，研究TFSG对TLR/MyD88/NF-κB通路与NLRP3/ASC/caspase-1轴关键蛋白的调控作用；并分别用激动（活）剂、诱变剂或质粒转染技术上调上述通路与轴关键蛋白的表达，研究TFSG抗GA新机制；为痛风发病机制研究和药物筛选提供新思路和新靶点。

At present, the morbidity rate of gout in China is 2.2%, which is similar to the western developed countries. Latest research data showed that TLR/MyD88/NF-κB signaling pathway and NLRP3/ASC/caspase-1 axis could active IL-lβ synergistically, which play a vital role in monosodium urate crystals (MSU) induced gouty arthritis. These data bring new opportunity for the development of drugs to treat gout. Our previous results showed that total flavonoids from Smilax glabra (TFSG) has obvious anti-gout effects, and could significantly inhibit the IL-1β secretion and NLRP3 inflammasome mRNA and protein expression in mouse bone marrow-derived macrophages (BMDMs) stimulated by MSU. This project aimed to study the regulatory mechanisms of TFSG to some key proteins in TLR/MyD88/NF-κB signaling pathway and NLRP3/ASC/caspase-1 axis by using modern molecular biotechnology techniques, associate with flow cytometry, confocal laser microscope, transmission electron microscope, and immunohistochemistry. Moreover, in order to study the new mechanism of TFSG to treat gouty arthritis, we use NF-κB agonist, NLRP3 activator, ROS inducer or plasmid transfection technique, to up-regulate the key proteins expression in above-mentioned signaling pathway and axis. This project could offer the innovative ideas and new targets to study the nosogenesis of gout and anti-gout drug screening.