Sözmen Sule Çağlayan, Kurul Semra Hız, Yiş Uluç, Tuğyan Kazım, Baykara Başak, Yılmaz Osman
Department of Pediatrics, School of Medicine, Dokuz Eylül University, İzmir, Turkey.
Brain Dev. 2012 Mar;34(3):189-95. doi: 10.1016/j.braindev.2011.05.002. Epub 2011 May 19.
Status epilepticus triggers a mixture of apoptotic and necrotic cell death within the hippocampus. This neuronal loss may result in the development of epilepsy and cognitive deficits. Erythropoietin mediates a number of biological actions within the central nervous system and has been shown to be neuroprotective. In the present study, we investigated the effects of recombinant human erythropoietin on hippocampus of rat after lithium-pilocarpine induced status epilepticus. Twenty-one dam reared Wistar male rats, 21-day-old were divided into three groups: control group, lithium-pilocarpine induced status epilepticus and lithium-pilocarpine induced status epilepticus and erythropoietin treated group. Erythropoietin treated group received recombinant human erythropoietin 10 U/g intraperitoneally 40 min after pilocarpine injection for 5 days. Rats were sacrificed and brain tissues were collected at 5th day of experiment. Neuronal cell death and apoptosis were evaluated. Histopathological examination showed that erythropoietin significantly decreased neuronal cell death in CA1, CA2, CA3 and dentate gyrus regions of hippocampus. It also diminished apoptosis in the CA1 and dentate gyrus regions of hippocampus. In conclusion, erythropoietin may preserve the number of neurons and decrease apoptosis in model of status epilepticus induced by lithium-pilocarpine. This experimental study suggests that erythropoietin administration may be neuroprotective in status epilepticus.
癫痫持续状态会引发海马体内凋亡性和坏死性细胞死亡的混合情况。这种神经元损失可能导致癫痫和认知缺陷的发展。促红细胞生成素介导中枢神经系统内的多种生物学作用，并且已被证明具有神经保护作用。在本研究中，我们调查了重组人促红细胞生成素对锂-匹罗卡品诱导的癫痫持续状态后大鼠海马体的影响。21只由母鼠饲养的21日龄雄性Wistar大鼠被分为三组：对照组、锂-匹罗卡品诱导的癫痫持续状态组以及锂-匹罗卡品诱导的癫痫持续状态并接受促红细胞生成素治疗的组。促红细胞生成素治疗组在注射匹罗卡品40分钟后腹腔注射10 U/g重组人促红细胞生成素，持续5天。在实验的第5天处死大鼠并收集脑组织。评估神经元细胞死亡和凋亡情况。组织病理学检查显示，促红细胞生成素显著减少了海马体CA1、CA2、CA3和齿状回区域的神经元细胞死亡。它还减少了海马体CA1和齿状回区域的凋亡。总之，在锂-匹罗卡品诱导的癫痫持续状态模型中，促红细胞生成素可能会保留神经元数量并减少凋亡。这项实验研究表明，给予促红细胞生成素在癫痫持续状态中可能具有神经保护作用。
