白细胞介素-1β在癫痫发病机制中的新作用
New roles for interleukin-1 Beta in the mechanisms of epilepsy.
机构信息
Department of Neuroscience, Mario Negri Institute for Pharmacological Research, Milano, Italy.
出版信息
Epilepsy Curr. 2007 Mar-Apr;7(2):45-50. doi: 10.1111/j.1535-7511.2007.00165.x.
Abstract
The mechanisms that transform a normal brain to an epileptic one are not fully understood. Interleukin-1 beta (IL-1beta) contributes to neuronal degeneration observed in several neurological disorders and recently has been implicated in neuronal injury that may accompany the process of epileptogenesis. This review presents the hypothesis that IL-1beta may contribute to the development of epilepsy via several mechanisms, including classical effects on neuronal survival and transcription pathways; novel rapid effects on receptor-gated ion channels; and long-lasting effects on expression of selective gene families. Thus, evidence that IL-1beta actions in epilepsy can be independent from the neurotoxic effects of this cytokine is presented.
摘要
将正常大脑转变为癫痫状态的机制尚未完全阐明。白细胞介素-1β（IL-1β）参与了几种神经疾病中观察到的神经元退化，最近还与癫痫发生过程中可能伴随的神经元损伤有关。这篇综述提出了一个假说，即 IL-1β 可能通过多种机制导致癫痫的发生，包括对神经元存活和转录途径的经典影响；对受体门控离子通道的新的快速影响；以及对特定基因家族表达的持久影响。因此，本文提出了这样一个证据，即 IL-1β 在癫痫中的作用可能与该细胞因子的神经毒性作用无关。
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