Abstract: Objective:To investigate the mechanism of Fructus Foeniculi(FF)’s anti-liver fibrosis based on network pharmacology-molecular docking.Methods:The active ingredients of FF were obtained by traditional Chinese medicine systems pharmacology analysis platform(TCMSP), and targets of active ingredients were obtained via Swiss Target Prediction platform.The disease targets were obtained by searching GeneCards and OMIM databases.The key targets were obtained by intersecting the active ingredient targets and disease targets.GO and KEGG analysis were performed by David database.The predicted results were verified by AutoDock Vina software and animal experiments.Results:9 active ingredients of FF and 115 key anti-liver fibrosis targets were obtained from the databases.The reversal of liver fibrosis might be related to the core components such as ammidin, beta-sitosterol, stigmasterol, anethole and anisaldehyde.It was speculated that FF regulated IL-17, PI3K-Akt, hepatitis B, non-alcoholic fatty liver, hepatitis B, AGE-RAGE and other signaling pathways through PTGS2, ESR1, MTOR, TLR4, PPARA and other core targets to exert anti-liver fibrosis effect.The results of molecular docking demonstrated that the core components of FF had good binding properties to the core protein targets, indicating good biological activity.Animal experiments further verified that FF exerted its anti-liver fibrosis effect by regulating PTGS2, ESR1, MTOR, TLR4, PPARA and other targets to alleviate inflammatory response and reduce extracellular matrix deposition.Conclusion:9 active core components, 5 key targets and signaling pathways of FF’s anti-liver fibrosis are systematically revealed through network pharmacology, molecular docking and animal experiments, which lays a good foundation for its future clinical application.