Purpose:　This　study　aimed　to　investigate　the　main　pharmacological　action　and　underlying　mechanisms　of　Jin　Gu　Lian　Capsule　(JGL)　against　rheumatoid　arthritis　(RA)　based　on　network　pharmacology　and　experimental　verification.Methods:　Network　pharmacology　approaches　were　performed　to　explore　the　core　active　compounds　of　JGL,　key　therapeutic　targets,　and　signaling　pathways.　Molecular　docking　was　used　to　predict　the　binding　affinity　of　compounds　with　targets.　In　vivo　experiments　were　undertaken　to　validate　the　findings　from　network　analysis.Results:　A　total　of　52　targets　were　identified　as　candidate　JGL　targets　for　RA.　Sixteen　ingredients　were　identified　as　the　core　active　compounds,　including,　quercetin,　myricetin,　salidroside,　etc.　Interleukin-1　beta　(IL1B),　transcription　factor　AP-1　(JUN),　growth-regulated　alpha　protein　(CXCL1),　C-X-C　motif　chemokine　(CXCL)3,　CXCL2,　signal　transducer　and　activator　of　transcription　1　(STAT1),　prostaglandin　G/H　synthase　2　(PTGS2),　matrix　metalloproteinase　(MMP)1,　inhibitor　of　nuclear　factor　kappa-B　kinase　subunit　beta　(IKBKB)　and　transcription　factor　p65　(RELA)　were　obtained　as　the　key　therapeutic　targets.　Gene　Ontology　and　Kyoto　Encyclopedia　of　Genes　and　Genomes　pathway　enrichment　analysis　showed　that　the　efficacy　of　JGL　was　functionally　involved　in　regulating　immune-mediated　inflammation,　in　which　IL-17/NF-kappa　B　signaling　was　recommended　as　one　of　the　main　pathways.　Molecular　docking　suggested　that　the　core　active　compounds　bound　strongly　to　their　respective　targets.　Experimentally,　JGL　treatment　mitigated　inflammation,　showed　analgesic　activity,　and　ameliorated　collagen-induced　arthritis.　Enzyme-linked　immunosorbent　assay　showed　that　JGL　effectively　reduced　the　serum　levels　of　cytokines,　chemokines,　and　MMPs.　Immunohistochemistry　staining　showed　that　JGL　markedly　reduced　the　expression　of　the　targets　in　IL-17/NF-kappa　B　pathway　including　IL-17A,　IL-17RA,　NF-kappa　B　p65,　C-X-C　motif　ligand　2,　MMP1　and　MMP13.　Conclusion:　This　investigation　provided　evidence　that　JGL　may　alleviate　RA　symptoms　by　partially　inhibiting　the　immune-mediated　inflammation　via　IL-17/NF-kappa　B　pathway.