Involvement of Spinal Cord Nuclear Factor kB Activation in A Rat Model of Persistent,Postoperative Pain Evoked by Skin/Muscle Incision and Retraction （SMIR）

Background： Persistent postoperative pain is common but the pathogenic mechanisms underlying it are under debate. Recent studies have implicated the activation of nuclear factor kappa B （NF-kB） in spinal for development of neuropathic and inflammatory pain. Aims： The aim of the present study was to investigate whether NF-kB also mediates hyperalgesia in persistent postoperative pain and potentially the pathogenesis of postoperative pain, by measuring NF-kB levels and assessing the anti-allodynic effect of NF-r.B inhibition by pyrrolidine dithiocarbamate （PDTC） in rats after skin/muscle incision and retraction （SMIR） injury. Methods： After rats received a SMIR surgery, mechanical allodynia were determined by von Frey filaments, and NF-kB p65 in the spinal cord was quantified to determine the level NF-KB expression at different time points after SMIR by western blotting. The NF-kB inhibitor PDTC was administered intrathecally at day 1 after surgery and then daily for 7 days to determine the role of NF-KB in postoperative pain, Results： A significant increase in level of NF-kB p65 was observed in the spinal cord from day 1 to day 7 after SMIR, Intrathecal injection of PDTC attenuated SMIR-induced mechanical allodynia from day 3 to day 12. Conclusions： SMIR-induced mechanical allodynia can be partially reversed by the NF-kB inhibitor. Our results suggest that NF-r.B activation in spinal cord plays a role in SMIR-induced mechanical allodyuia in rats. Therefore, NF-kB inhibition may be useful but not sufficient for the therapeutic control of postoperative pain,