We investigated the therapeutic effect of environmental enrichment (EE) on traumatic brain injury (TBI). Sixty 8-week-old SD rats were divided into four groups: sham-operated (sham group), sham + EE standard environment (STD), TBI group, and TBI + EE. Sham + EE and TBI + EE groups recovered in environmental enrichment areas after surgery, whereas the Sham and TBI groups recovered in STD. Modeling repeatability was assessed using acute neurology. The effect of EE on the differentiation of neural cells in the dentate gyrus of the hippocampus was analyzed using immunofluorescence, whereas the cognitive learning ability of rats was analyzed using the Morris water maze test. Brain damage based on cortical lesions was assessed using HE. The expression levels of vascular endothelial growth factor VEGF, three nerve growth factors, and three inflammatory factors in brain cortical tissue were analyzed using western blot. Fluorescence staining revealed that EE exerted its effect by promoting the proliferation of neuronal cells in the dentate gyrus of the rat hippocampus. The Morris water maze experiment showed that EE + TBI improved the cognitive function, learning, and memory of rats after brain injury. At 19 d, the cortical damage area of rats in the EE + TBI group had significantly reduced. Also, EE improved the cognitive function and long-term memory of rats. EE treatment further significantly increased NGF expression, neurotrophins-3, VEGF, BDNF, and IL-10 in the cerebral cortex after TBI. Also, EE significantly improved the nerve recovery and vascular structure in rats. IL-1β and TNF-α expression were lower in the EE + TBI group than in the EE group. In general, EE treatment can accelerate brain injury repair through revascularization, promotes the growth of residual neuronal axons, and improve neuroinflammation.