Curcumin Provides Neuroprotection After Spinal Cord Injury

Background. Traumatic spinal cord injury (SCI) is a major cause of long-term disability. However, therapeutic agents targeting SCI are sorely lacking. The aim of this study was to investigate whether curcumin has neuroprotective effects after SCI in rats. Materials and methods. Studies were performed in 39 male Sprague-Dawley rats after spinal cord hemisection. The animals were randomly divided into three groups: sham, vehicle, and curcumin. The Basso, Beattie, and Bresnahan (BBB) scale was used to evaluate functional outcome. Specimens were tested for histologic, terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL), and immunohistochemical staining. Primary cultured astrocytes were used to test the inhibitory effect of curcumin on glial reactivation. Results. TheBBBscoresfortheaffectedhindlimbafterhemisectionweresignificantlyimprovedinthecurcumin-treated group compared with the vehicle group (on d 3 and 7; P <0.001). Immunohistochemistry of NeuN revealed remarkable neuronal loss inthe vehicle group after hemisection. In comparison, curcumin significantly protected neurons after SCI (curcumin comparedwithvehicle;P <0.001).Furthermore,curcumin significantly attenuated apoptosis after SCI (curcumin compared with vehicle; P < 0.001). RT-PCR demonstrated that the expression ofglialfibrillary acidic protein (GFAP) was significantly inhibited by curcumin. Conclusions. Curcumin inhibited apoptosis and neuron loss, quenched astrocyte activation, and significantlyimprovedneurologicdeficit7dafterspinalcord hemisection. By down-regulating GFAP expression, curcumin seems to attenuate astrocyte reactivation, which may be beneficial for neuronal survival. This is