Previous studies have suggested that impairment secondary to mechanical injury is a major cause of irreversible damage to the spinal cord. Inflammatory chemokines have been shown to play an important role in the pathological and physiological consequences of secondary spinal cord injury (SCI). The aim of the present study was to evaluate how changes in the expression levels of the cellular chemokine, monocyte chemoattractant peptide-1 (MCP-1), and the chemotaxis of inflammatory cells (monocytes and macrophages) are involved in the process of SCI. RNA interference methods were used to study the mechanisms that protect residual neurons after SCI in an attempt to explore novel, early interventions for managing SCI. Our results suggested that inhibiting inflammation alleviates nerve cell injury caused by apoptosis and provides a potentially important approach for the future treatment of secondary SCI.