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Antiallodynic effects of microglial interleukin-1#x03B2; inhibition in the spinal cord

机译:微胶层白细胞介素-1β抑制在脊髓中的抗衰老效应

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Microglia play a pivotal role in synaptic plasticity of chronic pain. In this study, the potential role of interleukin 1beta (IL-1β), mainly released by microglia in early stage of nerve injury, in mechanical allodynia induced by tetanic stimulation of the sciatic nerve (TSS) was examined. Mechanical allodynia was observed on both ipsilateral and contralateral sides of TSS. Moreover, the expression of the microglial marker Iba-1 and the proinflammatory cytokine IL-1β were significantly increased. Intrathecal injection of the IL-1 receptor antagonist (IL-1ra, 3.5 µg/ml, 20 µl/rat) 30 min before TSS significantly inhibited bilateral mechanical allodynia on day 3, 5 and 7 after TSS. Immunohistochemistry showed that IL-1β was colocalized with the microglial marker OX-42 in the spinal superficial dorsal horn, but not with the astrocytic marker GFAP and the neuronal marker NeuN on day 4 following TSS. The results demonstrate that microglial IL-1β participates in the hypersensitivity of pain behaviors induced by TSS.
机译:微胶质细胞在慢性疼痛的突触可塑性中发挥着关键作用。在本研究中,检查了白细胞介素1Beta(IL-1β)的潜在作用,主要在神经损伤早期释放的MICRIGLIA释放,在由突科刺激坐骨神经(TSS)诱导的机械异常中。在TSS的同侧和对侧侧观察到机械异常性疼痛。此外,显微胶质标记物IBA-1和促炎细胞因子IL-1β的表达显着增加。在TSS在TSS之后的第3,5和7天显着抑制双侧机械异常,鞘内注射IL-1受体拮抗剂(IL-1RA,3.5μg/ ml,20μl/大鼠)30分钟。免疫组织化学表明,IL-1β在脊椎表面背角中与微胶质标记物OX-42分致大致,但在TSS之后的第4天,不含星形胶质标记GFAP和神经元标记Neun。结果表明,小胶囊IL-1β参与TSS诱导的疼痛行为的超敏反应。

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