First Department of Anesthesiology and Surgery, Affiliated Hospital of Shaanxi University of Traditional Chinese Medicine, Xianyang, Shaanxi, China.
J Cell Biochem. 2020 Mar;121(3):2277-2283. doi: 10.1002/jcb.29450. Epub 2019 Oct 31.
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.
神经病理性疼痛（NPP）是一种不良的病理性疼痛，具有痛觉过敏、感觉异常和自发性疼痛的特点。本研究旨在研究右美托咪定（Dex）对 NPP 的影响。通过慢性缩窄性损伤（CCI）手术形成 NPP 大鼠模型。通过定量逆转录聚合酶链反应或 Western blot 分别检测 OX42 和抗神经胶质纤维酸性蛋白（GFAP）、神经生长因子（NGFs）和 Janus 激酶/信号转导和转录激活因子（JAK/STAT）蛋白。通过酶联免疫吸附试验检测炎症因子。结果表明，Dex 明显缓解 CCI 刺激的机械性痛觉过敏和热痛觉过敏。同时，CCI 大鼠白细胞介素-1β、肿瘤坏死因子-α、趋化因子 C-X3-C 基序配体 1 和 C-C 基序趋化因子配体 2 的表达显著增加，但 Dex 可逆转这些作用。此外，Dex 促进 CCI 大鼠 NGF、脑源性神经营养因子、神经营养因子-3（NT-3）和 NT-4 的表达。此外，OX42 和 GFAP 的 RNA 或蛋白表达水平在 CCI 大鼠中显著增加，而 Dex 抑制了 OX42 和 GFAP 的表达。此外，Dex 通过减少 CCI 大鼠中的 p-JAK 和 p-STAT 来阻断 JAK/STAT 信号通路。Dex 通过调节 CCI 大鼠中的 JAK/STAT 通路具有缓解 NPP 的潜力。
