Abstract： Objective： To analyze the action mechanism of Zibu Jiechang Powder in treating ulcerative colitis （UC）based on network pharmacology and molecular docking techniques. Methods：Active components and predicted targets of Zibu Jiechang Powder were screened through the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform（TCMSP） and literature review. Relevant targets for UC were identified using the GeneCards， Online Mendelian Inheritance in Man（OMIM）， and Therapeutic Target Database（TTD）. Cytoscape 3.10.0 software was used to construct a "compound-drug-target-disease" network and a protein-protein interaction （PPI） network. Gene Ontology（GO） functional and Kyoto Encyclopedia of Genes and Genomes（KEGG） pathway enrichment analyses were performed using the DAVID database， and molecular docking was conducted for core components and targets. Results：A total of 54 active components，532 drug targets，and 3 646 disease targets were identified. Based on the topological analysis of the "compound-drug-target-disease" network and PPI network， key targets such as signal transducer and activator of transcription 3（STAT3）， interleukin（IL）-6， mitogen-activated protein kinase（MAPK）1， MAPK3， epidermal growth factor receptor（EGFR）， AKT serine / threonine kinase 1 （AKT1）， and heat shock protein 90 alpha family class A member 1（HSP90AA1）were identified， along with core components such as kaempferol，quercetin，and luteolin. GO enrichment analysis identified 1 124 entries，primarily involving inflammatory response and xenobiotic metabolic processes. KEGG pathway analysis identified 127 pathways， mainly involving the IL-17 and phosphatidylinositol-3-kinase（PI3K）- AKT signaling pathways. Molecular docking showed that the binding energies between key targets and core components were less than -5.0 kcal/mol， indicating stable binding. Conclusion： Zibu Jiechang Powder treats UC by acting on targets such as STAT3 and IL-6 through active components like quercetin，kaempferol，and luteolin，regulating the IL-17 and PI3K-AKT signaling pathways.