Spinal cord injury (SCI) induces a sustained neuroinflammatory response that exacerbates secondary tissue damage and limits functional recovery, yet therapeutic modulation of inflammation is constrained by poor cellular specificity and off‐target effects. Here, we show that graphene oxide (GO) nanosheets enable delivery of the BET inhibitor JQ1, forming a stable non‐covalent complex (GO:JQ1) that enhances anti‐inflammatory and neuroprotective efficacy. In vitro, GO:JQ1 was preferentially internalized by primary macrophages inducing a sustained immunomodulatory response. In a mouse model of contusive SCI, a single intralesional administration of GO:JQ1 significantly improved locomotor recovery, reduced neuropathic pain, and preserved corticospinal conduction, outperforming free JQ1 or GO alone. These functional improvements were accompanied by modulation of inflammatory and oxidative stress‐related gene expression, increased tissue sparing and neuronal survival at chronic stages post‐injury. The preferential uptake of GO nanosheets by phagocytic cells, provides a plausible mechanism for localized epigenetic modulation of the inflammatory microenvironment while limiting neuronal exposure. Together, these findings establish GO‐mediated delivery as a promising nanosheet‐based platform for targeted epigenetic immunomodulation and functional repair after SCI.