Department of Pharmacology, Wakayama Medical University, 811-1 Kimiidera, Wakayama, Wakayama 641-0012, Japan.
Curr Opin Pharmacol. 2012 Feb;12(1):55-61. doi: 10.1016/j.coph.2011.10.007. Epub 2011 Oct 21.
There has been recent evidence showing the correlation between neuroinflammation owing to the chemokine-cytokine network and neuropathic pain. Chemokines and cytokines are derived from several types of cells in the peripheral and central nervous systems following nerve injury, and are largely involved in the pathogenesis of neuropathic pain. The roles of typical inflammatory cytokines such as interleukin-1β have become the recent center of attention. There is growing evidence that inflammatory chemokines (CCL2, CCL3, and fractalkine) play pivotal roles in neuropathic pain. Further investigations concerning the functions of the chemokine-cytokine network-mediated regulation of neuroinflammation may lead to novel therapeutic strategies against intractable neuropathic pain.
最近有证据表明，神经炎症与趋化因子-细胞因子网络和神经病理性疼痛之间存在相关性。趋化因子和细胞因子源自外周和中枢神经系统的几种类型的细胞，在神经病理性疼痛的发病机制中起重要作用。典型炎症细胞因子（如白细胞介素-1β）的作用已成为最近的关注焦点。越来越多的证据表明，炎症趋化因子（CCL2、CCL3 和 fractalkine）在神经病理性疼痛中发挥关键作用。进一步研究趋化因子-细胞因子网络介导的神经炎症调节功能可能为治疗难治性神经病理性疼痛提供新的治疗策略。
