Alyu Feyza, Dikmen Miriş
1Department of Pharmacology,Faculty of Pharmacy,Anadolu University,Eskisehir,Turkey.
Acta Neuropsychiatr. 2017 Feb;29(1):1-16. doi: 10.1017/neu.2016.47. Epub 2016 Oct 3.
Epilepsy is a chronic neurological disease characterised with seizures. The aetiology of the most generalised epilepsies cannot be explicitly determined and the seizures are pronounced to be genetically determined by disturbances of receptors in central nervous system. Besides, neurotransmitter distributions or other metabolic problems are supposed to involve in epileptogenesis. Lack of adequate data about pharmacological agents that have antiepileptogenic effects point to need of research on this field. Thus, in this review, inflammatory aspects of epileptogenesis has been focussed via considering several concepts like role of immune system, blood-brain barrier and antibody involvement in epileptogenesis.
We conducted an evidence-based review of the literatures in order to evaluate the possible participation of inflammatory processes to epileptogenesis and also, promising agents which are effective to these processes. We searched PubMed database up to November 2015 with no date restrictions.
In the present review, 163 appropriate articles were included. Obtained data suggests that inflammatory processes participate to epileptogenesis in several ways like affecting fibroblast growth factor-2 and tropomyosin receptor kinase B signalling pathways, detrimental proinflammatory pathways [such as the interleukin-1 beta (IL-1β)-interleukin-1 receptor type 1 (IL-1R1) system], mammalian target of rapamycin pathway, microglial activities, release of glial inflammatory proteins (such as macrophage inflammatory protein, interleukin 6, C-C motif ligand 2 and IL-1β), adhesion molecules that are suggested to function in signalling pathways between neurons and microglia and also linkage between these molecules and proinflammatory cytokines.
The literature research indicated that inflammation is a part of epileptogenesis. For this reason, further studies are necessary for assessing agents that will be effective in clinical use for therapeutic treatment of epileptogenesis.
癫痫是一种以发作性症状为特征的慢性神经系统疾病。大多数全身性癫痫的病因尚不能明确确定，且发作被认为是由中枢神经系统受体紊乱遗传决定的。此外，神经递质分布或其他代谢问题也被认为与癫痫发生有关。缺乏关于具有抗癫痫发生作用的药物的充分数据表明该领域需要开展研究。因此，在本综述中，通过考虑免疫系统的作用、血脑屏障和抗体参与癫痫发生等几个概念，聚焦于癫痫发生的炎症方面。
我们对文献进行了循证综述，以评估炎症过程对癫痫发生的可能参与情况，以及对这些过程有效的有前景的药物。我们检索了截至2015年11月的PubMed数据库，无日期限制。
在本综述中，纳入了163篇合适的文章。获得的数据表明，炎症过程以多种方式参与癫痫发生，如影响成纤维细胞生长因子-2和原肌球蛋白受体激酶B信号通路、有害的促炎途径[如白细胞介素-1β（IL-1β）-白细胞介素-1受体1型（IL-1R1）系统]、雷帕霉素哺乳动物靶标途径、小胶质细胞活性、神经胶质炎症蛋白（如巨噬细胞炎症蛋白、白细胞介素6、C-C基序配体2和IL-1β）的释放、被认为在神经元和小胶质细胞之间的信号通路中起作用的黏附分子，以及这些分子与促炎细胞因子之间的联系。
文献研究表明炎症是癫痫发生的一部分。因此，有必要进一步开展研究，以评估对癫痫发生的临床治疗有效的药物。
