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 factoralpha (TNFalpha), and the duration of nociceptive behavioral responses was measured with a stopwatch timer within 30 min. Western blotting was used to explore the protein levels of ionized calcium binding adaptor molecule1 (IBA1), nuclear factorkappaB (NFkappaB) phosphorylatedp65, interleukin (IL)6 and IL1beta. We performed reverse transcriptionquantitative polymerase chain reaction and ELISA were performed to determine the mRNA and protein expression levels of IL6 and IL1beta, respectively. An MTT assay was conducted to detect BV2 cell viability. Oxyntomodulin was observed to attenuate TNFalphainduced pain hypersensitivity in mice, as well as the expression of IBA1, NFkappaB pp65, IL6 and IL1beta in the spinal cord. Oxyntomodulin exhibited no cytotoxicity on BV2 cells, and attenuated TNFalphainduced IL6 and IL1beta production and release in BV2 cells and culture medium, respectively. Collectively, we proposed oxyntomodulin to attenuate TNFalpha induced neuropathic pain associated with the release of glial cytokines IL6 and IL1beta via inhibiting the activation of the NFkappaB pathway.