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Severe postoperative pain remains a clinical problem that impacts patient's rehabilitation. The present work aims to investigate the role of Toll-like receptor-4 (TLR4) activation in wounded plantar tissue and dorsal root ganglion (DRG) in the genesis of postoperative pain and its underlying mechanisms. Postoperative pain was induced by plantar incision in rat hind paw. Plantar incision led to increased expression of TLR4 in ipsilateral L4/5 DRGs, which occurred after 2 hour and was persistent to the third day after surgery. Similar to the change in TLR4 expression, there was also significant increase in phosphorylated NF-κB p65 (p-p65) in DRGs after surgery. Immunofluorescence staining revealed that the increased expressions of TLR4 and p-p65 not only in neuronal cells, but also in satellite glial cells in DRG. Furthermore, the enhanced expressions of TLR4 and p-p65 were also detected in plantar tissues around the incision, which was observed starting at 2 hours and lasting until the third day after surgery. Prior intrathecal (i.t.) injections of TAK-242 (a TLR4-specific antagonist) or PDTC (a NF-κB activation inhibitor) dose-dependently alleviated plantar incision-induced mechanical allodynia and thermal hyperalgesia, and inhibited the increased expressions of p-p65, TNF-α and IL-1β in DRG. Prior subcutaneous (s.c.) plantar injection of TAK-242 or PDTC also ameliorated pain-related hypersensitivity following plantar incision. Moreover, the s.c. injection of TAK-242 or PDTC inhibited the increased expressions of p-p65, TNF-α and IL-1β not only in local wounded plantar tissue but also dramatically in ipsilateral L4/L5 DRGs. TLR4/NF-κB signaling activation in local injured tissue and DRG contribute to the development of postoperative pain via regulating proinflammatory cytokines release. Targeting TLR4/NF-κB signaling in local tissue at early stage of surgery may be an effective strategy for treatment of postoperative pain.

TLR4/NF-κB signaling activation in plantar tissue and dorsal root ganglion involves in the development of postoperative pain