Network Pharmacology-Based Exploration of the Mechanism of <i>Juncus effusus </i>in Treating Recurrent Oral Ulcer

目的：基于网络药理学和分子对接技术探究灯心草(Juncus effusus L.)治疗复发性口腔溃疡(Recurrent oral ulcer, ROU)的分子机制。方法：通过TCMSP、GeneCards和OMIM数据库预测灯心草活性成分与ROU相关靶点；利用Cytoscape 3.10.2软件构建“灯心草–成分–靶点–复发性口腔溃疡”网络及蛋白质相互作用(PPI)网络；采用R 4.4.1软件进行基因本体(GO)和京都基因与基因组百科全书(KEGG)信号通路富集分析；通过PyMOL 3.0.4和AutoDock Vina 1.5.7软件进行分子对接验证。结果：筛选出灯心草中13个活性成分及ROU相关2540个靶点，其中成分与疾病的共同靶点73个。GO和KEGG富集分析显示，靶点与炎症反应调控、氧化应激过程相关，主要涉及PI3K-AKT及IL-17信号通路。分子对接分析表明，核心成分与EGFR、MMP9、TP53、JUN、IL-6、CASP3、AKT1等靶点结合能均小于−5 kcal/mol，表明灯心草的成分靶点与ROU的核心靶点有强亲和力。结论：灯心草可能通过木犀草素和菲类成分靶向结合MMP9、TP53、JUN、IL-6、AKT1，调控PI3K-AKT及IL-17通路，抑制炎症因子释放、减轻氧化损伤并促进黏膜修复，从而治疗ROU。Objective: To explore the molecular mechanisms of Juncus effusus L. in the treatment of recurrent oral ulcer (ROU) based on network pharmacology and molecular docking techniques. Methods: Active components of Juncus effusus and ROU-related targets were predicted using the TCMSP, GeneCards, and OMIM databases. The “herb-compound-target-ROU” network and protein-protein interaction (PPI) network were constructed using Cytoscape 3.10.2. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed using R 4.4.1. Molecular docking validation was conducted using PyMOL 3.0.4 and AutoDock Vina 1.5.7. Results: A total of 13 active components of Juncus effusus and 2,540 ROU-related targets were identified, with 73 overlapping targets between the components and the disease. GO and KEGG enrichment analyses revealed that the targets were associated with the regulation of inflammatory responses and oxidative stress processes, primarily involving the PI3K-AKT and IL-17 signaling pathways. Molecular docking analysis demonstrated that the core components exhibited strong binding affinities (binding energy Juncus effusus and the core targets of ROU. Conclusion: Juncus effusus may exert therapeutic effects on ROU through luteolin and phenanthrene components targeting MMP9, TP53, JUN, IL-6, and AKT1, thereby regulating the PI3K-AKT and IL-17 pathways, suppressing inflammatory cytokine release, alleviating oxidative damage, and promoting mucosal repair.