Effects of FK866 treatment on NF-κB p65 activation. By Western blot analysis, we evaluated the phosphorylation of Ser536 on the NF-κB subunit p65 and nuclear NF-κB p65 to investigate the cellular mechanisms by which treatments may attenuate the development of SCI. SCI caused a significant increase in the phosphorylation of NF-κB p65 on Ser536 at 24 h after the injury (a, a1); instead the treatment with FK866 prevented significantly the activation of NF-κB (a, a1). Moreover, traslocation of NF-κB p65 subunit in the nuclear fractions of the spinal cord tissue were also significant increased at 24 h after SCI compared with the sham-operated mice (b, b1). The levels of NF-κB p65 protein were significantly reduced in the nuclear fractions of the spinal cord tissues from animals that had received FK866 treatment as shown in (b, b1). Immunoblotting in a, b are representative of one spinal cord of five analyzed. The results in a1 and b1 are expressed as mean ± S.E.M from five blots, *p < 0.01 vs sham, °p < 0.01 versus SCI + vehicle.