To investigate the effect of eriodictyol on dendritic cell(DC) maturation and the molecular mechanism, based on network pharmacology, the related targets for DC, immunosuppression and inflammatory response were obtained through multiple data platforms. Cytoscape 3.6.1 software was used to construct the active component-potential target network, and the String was used to construct the protein interaction(PPI) network. GO and KEGG enrichment analysis were performed using Metascape, and the molecular docking was performed using Autodock Vina software. DCs were treated with different concentrations(210 μM, 280 μM and 350 μM) of eriodictyolin the absence or presence of lipopolysaccharides(LPS). The expression of cell surface molecules was detected by flow cytometry, cytokine secretion was detected by ELISA, and matrix metalloprotein MMP9 expression was detected by Western blot. 96 related targets were screened, 72 of them related to DC, 14 of them related to immunosuppression, and 48 of them related to inflammatory response. The core targets included AKT1, SRC, MMP9 and MMP2, etc., which were involved in biological processes such as the oxidative stress and the cell migration and signaling pathways including pathways in cancer, Ras signaling pathway, EGFR tyrosine kinase inhibitor resistance, c-type lectin receptor signaling pathway and TNF signaling pathway. The molecular docking showed that eriodictyol had stronger binding effect with MMP9. In vitro, eriodictyol significantly suppressed LPS-induced DC maturation characterized by the decreased levels of CD40 (P<0.01), CD86 (P<0.001), TNF-α (P<0.001), IL-6 (P<0.001) and MMP9 (P<0.01). Eriodictyol inhibited the maturation and migration of DC through co-stimulatory molecules CD40 and CD86, pro-inflammatory cytokines TNF-α and IL-6, and MMP9.