Activation of spinal NF-КB mediates pain behavior induced by plantar incision.

A growing body of evidence indicates that the activation of nuclear factor kappa B (NF-κB) pathway was involved in neuropathic and inflammatory pain, however, the role of NF-κB in incisional pain is still unclear. Therefore, in this study, we investigated whether the activation of NF-κB in the spinal cord is involved in pain hypersensitivity after a plantar incision in the rat hind paw. After rats received a plantar incision surgery, mechanical allodynia and thermal hyperalgesia were determined by von Frey filaments and radiant heat, respectively. Western blot was used to determineNF-κB activation at different time points after incision. The NF-κB inhibitor pyrrolidinedithiocarbamate (PDTC) was administered intrathecally 30 min before hind paw plantar incision to determine the role of NF-κB in incision-induced pain. Our results showed that the expression level of NF-κB was significantly increased in spinal cord dorsal horn from 30 min to 3 days after the incision. Intrathecal pretreatment of PDTC attenuated incision-induced mechanical allodynia and thermal hyperalgesia. Furthermore, PDTC significantly reduced the expression level of c-Fos in the dorsal horn after plantar incision. Taken together, plantar incision-induced pain behaviors can be prevented by the NF-κB inhibitor. Our results suggest that the blockage of the NF-КB signaling pathway might represent a valuable alternative for treating postoperative pain.