Objective : Epidural fibrosis (EF) is a major contributor to postoperative morbidity following laminectomy (LAM). This study investigated the antifibrotic, anti-inflammatory, and anti-angiogenic effects of nintedanib (NIN), a multi-tyrosine kinase inhibitor, in a rat model of post-LAM EF. Methods : Twenty-one male Wistar albino rats were assigned to three groups : control, LAM, and LAM + NIN. The LAM procedure was performed at the L3 level. NIN administration, following LAM, was administered orally at a dose of 50 mg/kg/day for 28 days. Histopathological evaluations included Hematoxylin & Eosin staining for dura mater thickness and fibroblast density, and Masson's trichrome staining for collagen deposition and adhesion grading. α-smooth muscle actin (α-SMA) expression was evaluated using immunohistochemistry and reverse transcription-quantitative polymerase chain reaction. Gene expression of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), vascular endothelial growth factor (VEGF), platelet-derived growth factor receptor (PDGFR), and transforming growth factor-β1 (TGF-β1) was quantified to characterize inflammatory, angiogenic, and fibrogenic responses. Statistical comparisons were conducted using one-way analysis of variance or Kruskal-Wallis tests with appropriate post hoc analyses. Results : The LAM group exhibited marked post-LAM changes, including increased dura mater thickness (8.20±0.23 vs. 3.93±0.08 ㎛ in controls, p<0.0001), elevated fibroblast density (p=0.0006), severe collagen deposition, and high-grade epidural adhesions (grade 3, p=0.0006). NIN treatment attenuated these alterations, reducing dura mater thickness (4.80±0.20 ㎛; p<0.0001 vs. LAM), fibroblast density (p<0.01), and adhesion grade (grade 1, p=0.0012). α-SMA immunoreactivity was high in LAM (grade 3, p<0.0001), whereas NIN significantly suppressed myofibroblast activation (grade 1, p=0.0012). NIN also significantly downregulated inflammatory mediators TNF-α (p<0.001) and IL-1β (p<0.001), as well as angiogenic markers VEGF (p<0.001) and PDGFR (p<0.001), and fibrogenic mediators TGF-β1 (p<0.001) and α-SMA (p<0.01). These findings indicate that NIN suppresses fibroblast activation, extracellular matrix accumulation, and myofibroblast differentiation, thereby limiting epidural adhesion and scar maturation. Conclusion : Nintedanib effectively mitigated epidural fibrosis after LAM through combined antifibrotic, anti-inflammatory, and anti-angiogenic actions. By improving the dural structure and reducing key molecules that contribute to scar formation, NIN shows significant promise as a treatment to prevent postoperative epidural adhesions. Future studies with extended follow-up may help clarify its clinical relevance.