Our main findings are as follows: (1) rosiglitazone attenuated established BCP by activating PPAR-γ in the spinal cord, which was reversed by the PPAR-γ antagonist GW9662; (2) rosiglitazone increased PPAR-γ expression in the spinal cord neurons of BCP rats; (3) tumor cell inoculation induces the activation of the NF-κB/NLRP3 inflammatory axis in the spinal cord dorsal horn neurons of BCP rats; and (4) rosiglitazone inhibited the NF-κB/NLRP3 inflammatory axis in spinal cord neurons by activating PPAR-γ to attenuate BCP. Here, NFKB1 is linked to neoplasm.