Icariin is a type of flavonoid derived from the Chinese herbal plant Epimedium sagittatum Maxim. Mounting evidence has confirmed the beneficial effects of icariin in neurological diseases, including spinal cord injury (SCI). The aim of the present study was to investigate the neuroprotective effects of icariin in SCI and the precise underlying mechanism. The weight‑drop injury technique was applied to construct an SCI model in Sprague‑Dawley rats. Icariin (35 µmol/kg) was administered orally once daily for 7 consecutive days to examine its neuroprotective effects. The Basso, Beattie and Bresnahan scoring system was used for neurobehavioral evaluation. The water content of the injured spinal cord was measured via the dry‑wet weight method. Biochemical indices were examined by colorimetric assay using commercially available kits. Western blot analysis was used to detect protein expression. Icariin significantly accelerated the recovery of the locomotor function of SCI rats and decreased spinal cord water content. Icariin also attenuated SCI‑induced pro‑apoptotic protein expression and activity, while it increased anti‑apoptotic protein levels. In addition, icariin alleviated oxidative stress in SCI rats and decreased the levels of inflammatory molecules, including interleukin (IL)‑1β, IL‑6, tumor necrosis factor‑α, nitric oxide, nuclear factor‑κB and inducible nitric oxide synthase, and increased the expression of anti‑inflammatory proteins, including NADPH‑quinone oxidoreductase‑1, heme oxygenase‑1 and nuclear factor erythroid 2‑related factor 2 in the injured spinal cord. Therefore, icariin treatment accelerated locomotor function recovery in SCI, and its protective effects may be mediated via its antioxidant, anti‑inflammatory and anti‑apoptotic bioactivity.