Dexmedetomidine alleviates neuropathic pain by regulating JAK/STAT pathway in rats.

Neuropathic pain (NPP) is an unfavorable pathological pain with the characteristics of hyperalgesia, allodynia, and spontaneous pain. This study aimed to study the influence of dexmedetomidine (Dex) on NPP. Chronic constriction injury (CCI) was operated to form the NPP rat model. The OX42 and anti-glial fibrillary acidic protein (GFAP), the nerve growth factors (NGFs), and the Janus kinase/signal transducers and activators of transcription (JAK/STAT) proteins were separately detected by quantitative reverse transcription-polymerase chain reaction or Western blot. Inflammatory factors were detected by enzyme-linked immunosorbent assay. The results demonstrated that Dex obviously alleviated CCI-stimulated mechanical allodynia and thermal hyperalgesia. Meanwhile, the expressions of interleukin-1β, tumor necrosis factor-α, chemokine c-X3-c-motif ligand 1, and C-C motif chemokine ligand 2 were greatly increased in CCI rats, but these effects were reversed by Dex. In addition, Dex promoted the expressions of NGF, brain-derived neurotrophic factor, neurotrophins-3 (NT-3), and NT-4 in CCI rats. Moreover, the RNA or protein expression levels of OX42 and GFAP were significantly increased in CCI rats, while Dex inhibited the expressions of OX42 and GFAP. Furthermore, Dex blocked JAK/STAT signaling pathway by decreasing p-JAK and p-STAT in CCI rats. Dex had the potential to alleviate NPP by regulating JAK/STAT pathway in CCI rat.