目的 通过整合网络药理学和网络毒理学，探究合欢皮抗焦虑的治疗机制和导致肾损伤的致毒机制。方法 基于ETCM、TCMID和BATMAN-TCM数据库收集合欢皮化学成分，并通过文献检索对合欢皮的生物活性成分进行筛选和补充。基于PharmMapper、SwissTargetPrediction、BATMAN-TCM和ETCM数据库获取成分对应靶点；在CTD和GeneCards数据库中检索得到焦虑症和肾毒性相关靶点，分别与药物靶点取交集得到药效和毒性共有靶点；将共有靶点导入STRING数据库进行蛋白互作分析，在Cytoscape软件进行可视化分析；采用STRING数据库进行GO生物分析和KEGG通路富集分析。结果 筛选得到生物活性成分共51个，对应靶点747个，其与焦虑症和肾毒性交集靶点分别为134、144个，相关通路分别为173、184条。合欢皮可通过调控cAMP、RAS、MAPK、雌激素、催乳素、甲状腺激素和TNF等信号途径治疗焦虑症；其肾毒性的产生与BCL2、SOD靶点以及VEGF、MAPK、mTOR、PI3K-Akt、HIF-1、TNF、Toll-like、NOD-like等信号通路关系密切。结论 发现合欢皮抗焦虑成分主要为木脂素及黄酮类化合物，致毒成分主要为皂苷类化合物。抗焦虑作用可能通过影响神经递质5-HT以及下丘脑-垂体-肾上腺（HPA）轴、下丘脑-垂体-性腺（HPG）轴、下丘脑-垂体-甲状腺（HPT）轴发挥作用，并通过诱导炎症反应、缺氧状态、异常凋亡、氧化应激反应和自噬失衡产生肾毒性。

Objective To explore the anxiolytic effects mechanism and nephrotoxicity mechanism of Albizia Cortex by integrating network pharmacology and network toxicology. Methods The chemical components of Albizia Cortex was collected from ETCM, TCMID and BATMAN-TCM databases. The bioactive constituents of Albizia Cortex were screened and supplemented by literature search. The corresponding targets were obtained from PharmMapper, SwissTargetPrediction, BATMAN-TCM and ETCM databases. The anxiety disorder targets and nephrotoxicity targets which were obtained from the CTD and GeneCards databases were intersected with drugs targets separately and introduced into the STRING database to construct the protein interaction network diagram. Visual analysis was carried out in Cytoscape, and GO biological process and KEGG enrichment analysis were carried out in the STRING database. Results A total of 51 bioactive compounds were obtained, corresponding to 747 targets. There were 134 cross-targets and 173 related pathways in anxiety, 144 cross-targets and 184 related pathways in nephrotoxicity. The results show that the Albizia Cortex could regulate the cAMP, Ras, MAPK, Estrogen, Prolactin, Thyroid hormone and TNF pathways to treat anxiety disorders. Nephrotoxicity is closely related to BCL2, SOD targets and VEGF, MAPK, mTOR, PI3K-Akt, HIF-1,TNF,Toll-like, NODlike pathways. Conclusion The study found that the anxiolytic components of Albizia Cortex were mainly lignans and flavonoids, and the toxic components were mainly saponins. The anxiolytic effect probably influenced the 5-HT and HPA, HPG, HPT, and induce nephrotoxicity by inducing inflammation, hypoxia, abnormal apoptosis, oxidative stress and autophagy imbalance.