<scp>LipoxinA₄</scp> induced antinociception and decreased expression of <scp>NF‐κB</scp> and pro‐inflammatory cytokines after chronic dorsal root ganglia compression in rats

<jats:title>Abstract</jats:title><jats:p>Inflammatory and immune responses following nerve injury have been shown to play an important role in neuropathic pain. Lipoxins are endogenous lipoxygenase‐derived eicosanoids performing protective roles in a range of pathophysiologic processes. Here, we examined the effects of intrathecal <jats:styled-content style="fixed-case">lipoxinA4</jats:styled-content> (<jats:styled-content style="fixed-case">LXA4</jats:styled-content>) on <jats:styled-content style="fixed-case">NF‐κB</jats:styled-content> activation and pro‐inflammatory cytokine (<jats:styled-content style="fixed-case">TNF‐α</jats:styled-content>, <jats:styled-content style="fixed-case">IL‐1β</jats:styled-content> and <jats:styled-content style="fixed-case">IL‐6</jats:styled-content>) expression in dorsal root ganglia (<jats:styled-content style="fixed-case">DRG</jats:styled-content>) following chronic compression of <jats:styled-content style="fixed-case">DRG</jats:styled-content> (<jats:styled-content style="fixed-case">CCD</jats:styled-content>), a model of neuropathic pain. Daily intrathecal injection of vehicle or <jats:styled-content style="fixed-case">LXA4</jats:styled-content> (10 ng or 100 ng) was performed for three successive days post‐<jats:styled-content style="fixed-case">CCD</jats:styled-content>. <jats:styled-content style="fixed-case">CCD</jats:styled-content> induced both mechanical allodynia and thermal hyperalgesia, and increased the expression of <jats:styled-content style="fixed-case">TNF‐α</jats:styled-content>, <jats:styled-content style="fixed-case">IL‐1β</jats:styled-content>, <jats:styled-content style="fixed-case">IL‐6</jats:styled-content> and <jats:styled-content style="fixed-case">NF‐κB</jats:styled-content>. Intrathecal injection of <jats:styled-content style="fixed-case">LXA4</jats:styled-content> prevented the development of neuropathic pain and inhibited <jats:styled-content style="fixed-case">NF‐κB</jats:styled-content> activation and pro‐inflammatory cytokine upregulation in a dose‐dependent manner. In this study, we have shown the strong protective effect of intrathecal <jats:styled-content style="fixed-case">LXA4</jats:styled-content> on the development of nociceptive behaviors induced by <jats:styled-content style="fixed-case">CCD</jats:styled-content> and that these effects might be associated with its anti‐inflammatory and pro‐resolution properties.</jats:p>