Network Pharmacology and Molecular Docking Reveal the Mechanism of Rhizoma Drynariae Against Rotator Cuff Injury.

Rotator cuff injury (RCI) is a refractory musculoskeletal disorder marked by chronic inflammation, tenocyte apoptosis, impaired angiogenesis, and extracellular matrix (ECM) dysregulation, with limited clinical treatments available. This study employed network pharmacology and molecular docking to systematically investigate the active components, key targets, and signaling pathways of Rhizoma Drynariae (RD) against RCI. Eighteen active ingredients of RD and 213 non‑redundant targets were identified from TCMSP, ETCM, and SymMap, while 870 RCI‑related targets were retrieved from GeneCards and OMIM, yielding 71 overlapping candidate targets. Protein-protein interaction network analysis and cytoHubba screening revealed ten hub genes, including TNF, IL6, VEGFA, PTGS2, CASP3, AKT1, CCL2, PPARG, MAPK3, and HMOX1. Gene Ontology enrichment highlighted inflammatory response, oxidative stress, angiogenesis, cell proliferation, and ECM organization, while KEGG pathway analysis implicated the TNF, PI3K‑Akt, MAPK, and HIF‑1 signaling pathways. Molecular docking confirmed stable high‑affinity binding of eriodictyol, luteolin, catechin, naringenin, and aureusidin to these core proteins. Collectively, RD exerts anti‑RCI effects through a multi‑component, multi‑target, and multi‑pathway network, potentially alleviating RCI by suppressing inflammation and apoptosis, promoting angiogenesis, and enhancing ECM repair, thereby providing a theoretical foundation for its clinical application and experimental validation.