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首页> 外文期刊>Current Immunology Reviews >Cellular and Molecular Regulation of Inflammatory Pain, Nociception and Hyperalgesia - The Role of the Transcription Factor NF-κB as the Lynchpin Nocisensor: Hyperalgesic or Analgesic Effect?
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Cellular and Molecular Regulation of Inflammatory Pain, Nociception and Hyperalgesia - The Role of the Transcription Factor NF-κB as the Lynchpin Nocisensor: Hyperalgesic or Analgesic Effect?

机译：炎性疼痛，伤害感受和痛觉过敏的细胞和分子调控-转录因子NF-κB作为Lynchpin痛觉传感器的作用：痛觉过敏或镇痛作用？

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摘要

The milieu of inflammatory cells and inflammatory mediators is crucially involved in the genesis, persistence and severity of pain following trauma, infection or nerve injury. The mechanisms and pathways mediating pain and nociception (hyperalgesia) are transcriptionally regulated. The transcriptional mediator nuclear factor (NF)-κB plays a major role in regulating inflammatory responses, ostensibly via the control of gene expression/suppression. An association has recently emerged to establish a possible link between NF-κB and painociception, purportedly through the regulation of the inflammatory loop and the secretion (biosynthesis) of pro-inflammatory mediators. Current concepts conspicuously indicate that the effective inhibition of this transcription factor and associated upstream kinase(s) and the pathways that regulate its nuclear translocation could be major targets in a new strategy for the alleviation of inflammation and inflammatory- related pain. In contrast, recent evidence has implicated NF-κB in analgesic effects; the mechanisms are yet to be elucidated. To better understand this relationship, therefore, between NF-κB and the evolution of pain and hyperalgesia/ nociception, it is imperative to unravel the molecular basis of this process. This survey integrates current themes pertaining to the pivotal role that NF-κB shares in regulating pain through the decoding of implicated molecular pathways and signaling mechanisms.
机译：炎性细胞和炎性介质的环境至关重要地涉及创伤，感染或神经损伤后疼痛的发生，持续性和严重性。介导疼痛和伤害感受（痛觉过敏）的机制和途径受到转录调控。转录介质核因子（NF）-κB表面上通过控制基因表达/抑制，在调节炎症反应中起主要作用。最近出现了一种联系，据称是通过调节炎症环和促炎性介质的分泌（生物合成）来建立NF-κB与疼痛/伤害感受之间的可能联系。当前概念明显表明，在减轻炎症和与炎症相关的疼痛的新策略中，有效抑制这种转录因子和相关的上游激酶以及调节其核易位的途径可能是主要目标。相反，最近的证据表明NF-κB具有止痛作用。机制尚待阐明。因此，为了更好地理解NF-κB与疼痛和痛觉过敏/伤害感受的演变之间的关系，必须弄清该过程的分子基础。这项调查整合了与主题相关的当前主题，这些主题涉及NF-κB通过牵连的分子途径和信号传导机制的解码在调节疼痛中发挥的关键作用。

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