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首页> 外文期刊>European Journal of Pharmacology: An International Journal >Intrathecal administration of clonidine attenuates spinal neuroimmune activation in a rat model of neuropathic pain with existing hyperalgesia.
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Intrathecal administration of clonidine attenuates spinal neuroimmune activation in a rat model of neuropathic pain with existing hyperalgesia.

机译：鞘内注射可乐定可减轻现有痛觉过敏的神经性疼痛大鼠模型的脊髓神经免疫激活。

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摘要

Central neuroimmune activation contributes to the initiation and maintenance of neuropathic pain after nerve injury. The current study was aimed to examine the modulation of neuroimmune activation in the spinal cord by the alpha(2) adrenoceptor agonist, clonidine, in a rat model of neuropathic pain induced by partial sciatic nerve ligation (PSNL). Animals were randomly assigned into 6 groups: sham-operation with 20 microg clonidine or saline; and PSNL with clonidine (5, 10, and 20 microg) or saline. Fourteen days post-operation, various doses of clonidine or saline were injected intrathecally. The paw pressure threshold and paw withdrawal latencies were measured before and at 30, 60, 90, and 120 min after the injection of clonidine. Glial activation markers such as macrophage antigen complex-1 (mac-1) and glial fibrillary acidic protein (GFAP), interleukin (IL)-1beta and IL-6, nuclear factor-kappa B (NF-kappaB) activation, and p-p38 mitogen-activated protein kinase (MAPK) activation in the lumbar spinal cord were determined as well. Administration of clonidine resulted in a dose-dependent attenuation in PSNL-induced mechanical and thermal hyperalgesia. Furthermore, clonidine could markedly inhibit neuroimmune activation characterized by glial activation, production of cytokines, NF-kappaB activation as well as p38 activation. The antihyperalgesic effect of intrathecal clonidine in rats receiving PSNL might partly attribute to the inhibition of neuroimmune activation associated with the maintenance of neuropathic pain.
机译：中枢神经免疫激活有助于神经损伤后神经性疼痛的发生和维持。当前的研究旨在检查由部分坐骨神经结扎（PSNL）引起的神经性疼痛的大鼠模型中的alpha（2）肾上腺素能受体激动剂可乐定对脊髓中神经免疫激活的调节作用。将动物随机分为6组：用20微克可乐定或盐水进行假手术;将它们分为两组。 PSNL和可乐定（5、10和20微克）或盐水。术后十四天，鞘内注射各种剂量的可乐定或盐水。在注射可乐定之前和之后的30、60、90和120分钟测量爪压力阈值和爪退缩潜伏期。神经胶质激活标志物，例如巨噬细胞抗原复合物1（mac-1）和神经胶质纤维酸性蛋白（GFAP），白介素（IL）-1beta和IL-6，核因子-κB（NF-kappaB）激活和p-还确定了腰脊髓中的p38丝裂原活化蛋白激酶（MAPK）活化。可乐定的施用导致PSNL诱导的机械和热痛觉过敏的剂量依赖性衰减。此外，可乐定可显着抑制神经免疫激活，其特征是神经胶质激活，细胞因子产生，NF-κB激活以及p38激活。鞘内可乐定在接受PSNL的大鼠中的抗痛觉过敏作用可能部分归因于与维持神经性疼痛相关的神经免疫激活的抑制。

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