Abstract： Objective： To explore the action mechanism of Xitongkang in treating knee osteoarthritis （KOA） based on network pharmacology and molecular docking. Methods： The active components and related targets of Xitongkang were identified by the TCMSP platform， BATMAN-TCM platform， UniProt， and GeneCards databases. KOA disease targets were collected from the GeneCards，NCBI，OMIM，and DrugBank databases. Medicine-disease intersecting targets were screened，and data visualization and PPI network construction were performed. GO and KEGG pathway enrichment analyses were conducted to explore possible mechanisms， and molecular docking was used for validation. Results： Visualization analysis of the "Xitongkang-main components-targets-KOA" regulatory network identified 26 components involved in the treatment of KOA. PPI network interaction construction and core target analysis identified the top 10 core targets with the strongest interactions： serine/threonine kinase 1 （AKT1）， vascular endothelial growth factor A （VEGFA）， interleukin-1β （IL-1β）， tumor protein p53 （TP53）， epidermal growth factor （EGF）， matrix metalloproteinase 9 （MMP9），caspase-3 （CASP3），hypoxia-inducible factor 1α （HIF-1α）， prostaglandin-endoperoxide synthase 2 （PTGS2）， and myelocytomatosis proto-oncogene （MYC）. GO enrichment analysis mainly involved biological processes such as response to lipopolysaccharide， bacterial molecules， oxidative stress， radiation response， and nutrient levels. KEGG pathway enrichment indicated that interleukin-17 （IL-17）， tumor necrosis factor （TNF）， advanced glycation end products-receptor for advanced glycation end products （AGERAGE）， and p53 protein （p53） signaling pathways might be closely related to KOA. Molecular docking results showed that the binding energies between core components and core targets were all less than -5 kcal/mol. Conclusion： Xitongkang may exert its therapeutic effects on KOA through active components such as quercetin， luteolin， kaempferol， naringin， and acacetin， acting on targets like AKT1， VEGFA， and IL-1β， and regulating signaling pathways such as IL-17，TNF，AGE-RAGE，and p53.