摘要Epimedium Herba(EH)demonstrates significant therapeutic potential against prostate can-cer(PC),though its mechanisms of action remain incompletely understood.This study invest-igates the pharmacological mechanisms of EH in treating PC through network pharmacology analysis and experimental validation.Active components and potential targets of EH were identified using network pharmacology from the Traditional Chinese Medicine Systems Phar-macology Database and Analysis Platform(TCMSP).The STRING database facilitated the con-struction of a protein-protein interaction(PPI)network for shared targets and the identifica-tion of core anti-PC targets.Messenger ribonucleic acid(mRNA)and protein expression of core target genes in normal prostate and PC tissues,along with their correlation to overall PC survival,were analyzed using The Cancer Genome Atlas(TCGA),Human Protein Atlas(HPA),and Gene Expression Profiling Interactive Analysis(GEPIA)databases.Gene ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway enrichment analyses were performed on the potential targets.Molecular docking of quercetin with key targets(TP53,TNF,heat shock protein 90 alpha family class A member 1(HSP90AA1),AKT1,CASP3,and ESR1)was conducted,with results visualized using PyMOL.In vitro experiments validated the network pharmacology predictions.Twenty-three active ingredients of EH were identified,and the intersection of potential targets with PC targets yielded 183 potential targets.PPI net-work analysis revealed six key genes:targets(TP53),TNF,HSP90AA1,AKT1,CASP3,and ESR1.GO enrichment analysis identified 2369 biological processes(BP),77 cellular components(CC),and 215 molecular functions(MF).KEGG pathway enrichment analysis demonstrated that EH's anti-cancer effects were mediated through interleukin-17(IL-17),TNF,phos-phatidylinositol 3-kinase(PI3K)-AKT,apoptosis,p53,HIF-1,mitogen-activated protein kinase(MAPK),nuclear factor κB(NF-κB),and EGFR tyrosine kinase inhibitor resistance pathways.Core target validation confirmed consistency with the study's findings.Molecular docking in-dicated stable binding between the six core targets and quercetin.In vitro experiments con-firmed quercetin's inhibition of proliferation and induction of apoptosis in ACT-1 cells.This investigation identifies potential therapeutic targets for PC through network pharmacology and experimental validation.