目的 基于网络药理学探索防己治疗痛风性关节炎的作用机制及物质基础。方法 制备防己的水提取物冻干粉，随后运用液质联用技术分析其中的化学成分。使用SwissTargetPrediction数据库预测防己化学成分的靶点。在GeneCards数据库和CTD数据库中检索痛风性关节炎的相关靶点。使用Venny 2.1.0对化学成分靶点及痛风性关节炎的相关靶点进行交集分析。运用DAVID数据库分析上述具有交集联系的靶点的KEGG通路。使用Cytoscape软件构建防己的化学成分-痛风性关节炎靶点-通路的关联网络。运用尿酸钠诱导的痛风性关节炎模型对网络药理学分析结果进行验证。结果 通过液质联用技术鉴别了防己中的63个化学成分。其中的17个化学成分有可能干预痛风性关节炎的19个靶点，其中的9个靶点参与了4个关键性通路。在验证性实验中，防己水提取物冻干粉可以逆转大鼠滑膜中由尿酸钠诱导的一氧化氮合成酶2及基质金属肽酶1的异常表达。结论 网络药理学可以用于防己治疗痛风性关节炎的作用机制及物质基础的分析。防己中的多个化学成分主要影响了痛风性关节炎的凋亡、炎症、血管新生及尿酸清除过程。

Objective To explore the mechanism and material basis of Stephania tetrandra S. Moore (ST) in the treatment of gouty arthritis (GA) based on network pharmacology.Methods The freeze-dried powder of water extract of ST was prepared, and then the compounds were analyzed by liquid-mass spectrometry. SwissTargetPrediction database was used to predict the target of the compounds of ST. The relevant targets of GA were searched from GeneCards database and CTD database. Venny 2.1.0 was used to analyze the intersection of compound targets and the related targets for GA. The KEGG pathway of the above targets was analyzed by DAVID database. Cytoscape software was used to construct the association network of compounds-targets of GA-pathways of ST. The results of network pharmacological analysis were verified by using the gouty arthritis model induced by monosodium urate.Results A total of 63 compounds were identified by liquid-mass spectrometry. Seventeen of these compounds had the potential to interfere with 19 targets of GA, nine of which were involved in four key pathways. In the verification experiment, the freeze-dried powder of water extract of ST could reverse the abnormal expression of NOS2 and MMP1 induced by monosodium urate in rat synovial membrane.Conclusion The network pharmacology can be used to analyze the mechanism and material basis of ST in the treatment of GA. Several compounds from ST mainly affect the apoptosis, inflammation, angiogenesis, and uric acid clearance processes of GA.