Wilcox Karen S, Vezzani Annamaria
Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, UT, 84108, USA,
Adv Exp Med Biol. 2014;813:169-83. doi: 10.1007/978-94-017-8914-1_14.
Inflammation in the central nervous system (CNS) is associated with epilepsy and is characterized by the increased levels of a complex set of soluble molecules and their receptors in epileptogenic foci with profound neuromodulatory effects. These molecules activate receptor-mediated pathways in glia and neurons that contribute to hyperexcitability in neural networks that underlie seizure generation. As a consequence, exciting new opportunities now exist for novel therapies targeting the various components of the immune system and the associated inflammatory mediators, especially the IL-1β system. This review summarizes recent findings that increased our understanding of the role of inflammation in reducing seizure threshold, contributing to seizure generation, and participating in epileptogenesis. We will discuss preclinical studies supporting the hypothesis that pharmacological inhibition of specific proinflammatory signalings may be useful to treat drug-resistant seizures in human epilepsy, and possibly delay or arrest epileptogenesis.
中枢神经系统（CNS）中的炎症与癫痫相关，其特征是在致痫灶中一组复杂的可溶性分子及其受体水平升高，具有深远的神经调节作用。这些分子激活神经胶质细胞和神经元中受体介导的信号通路，导致构成癫痫发作基础的神经网络兴奋性过高。因此，针对免疫系统的各个组成部分和相关炎症介质，特别是白细胞介素-1β系统的新型疗法现在有了令人兴奋的新机会。本综述总结了最近的研究结果，这些结果加深了我们对炎症在降低癫痫发作阈值、促成癫痫发作以及参与癫痫发生中所起作用的理解。我们将讨论临床前研究，这些研究支持这样一种假设，即对特定促炎信号进行药理抑制可能有助于治疗人类癫痫中的耐药性癫痫发作，并可能延缓或阻止癫痫发生。
