Oxyntomodulin attenuates TNF‑α induced neuropathic pain by inhibiting the activation of the NF‑κB pathway

Neuropathic pain is rarely diagnosed. Oxyntomodulin is peripherally and centrally distributed; however, the potential mechanisms underlying the effects of oxyntomodulin in attenuating nociception remain unclear; thus, we aimed to explore them in the present study. A neuropathic pain model in male C57BL/6 mice was induced by intrathecal injection of tumor necrosis factor‑α (TNF‑α), and the duration of nociceptive behavioral responses was measured with a stop‑watch timer within 30 min. Western blotting was used to explore the protein levels of ionized calcium binding adaptor molecule‑1 (IBA1), nuclear factor‑κB (NF‑κB) phosphorylated‑p65, interleukin (IL)‑6 and IL‑1β. We performed reverse transcription‑quantitative polymerase chain reaction and ELISA were performed to determine the mRNA and protein expression levels of IL‑6 and IL‑1β, respectively. An MTT assay was conducted to detect BV2 cell viability. Oxyntomodulin was observed to attenuate TNF‑α‑induced pain hypersensitivity in mice, as well as the expression of IBA1, NF‑κB p‑p65, IL‑6 and IL‑1β in the spinal cord. Oxyntomodulin exhibited no cytotoxicity on BV2 cells, and attenuated TNF‑α‑induced IL‑6 and IL‑1β production and release in BV2 cells and culture medium, respectively. Collectively, we proposed oxyntomodulin to attenuate TNF‑α induced neuropathic pain associated with the release of glial cytokines IL‑6 and IL‑1β via inhibiting the activation of the NF‑κB pathway.