Effects of valproate sodium on extracellular signal-regulated kinase 1/2 phosphorylation following hippocampal neuronal epileptiform discharge in rats.
Effects of valproate sodium on extracellular signal-regulated kinase 1/2 phosphorylation following hippocampal neuronal epileptiform discharge in rats.
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DOI：
10.3892/etm.2013.1343
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发表时间：
2013-12
影响因子：
2.7
通讯作者：
Xu P
中科院分区：
文献类型：
--
作者：
Xu Z;Zhang J;Lei X;Xu Z;Peng Y;Yao B;Xu P
本研究旨在探讨丙戊酸钠（VPAS）对大鼠海马神经元癫痫样放电后细胞外信号调节激酶1/2（ERK1/2）磷酸化的影响。研究使用出生至少24小时的新生雌性和雄性斯普拉格-道利（SD）大鼠的神经元，将其快速断头处死。癫痫样放电细胞模型构建成功后，将神经元分为两组，即VPAS组和对照组。在浓度 - 效应实验中，在癫痫样放电前30分钟，用三种不同浓度（50、75和100毫克/升）的VPAS孵育神经元。采用免疫荧光技术检测磷酸化ERK1/2（p - ERK1/2）的表达。在时间 - 效应实验中，用VPAS（50毫克/升）孵育神经元，并在不同时间点（癫痫样放电前30分钟以及癫痫样放电后0分钟、30分钟、2小时和6小时）进行监测，采用蛋白质免疫印迹法检测p - ERK1/2蛋白表达的变化。在浓度 - 效应实验中，未发现不同浓度VPAS处理的神经元中p - ERK1/2的表达存在显著差异。然而，在时间 - 效应实验中，癫痫样放电前30分钟p - ERK1/2的表达明显低于其他时间点。此外，50毫克/升的VPAS能够降低神经元癫痫样放电的动作电位频率。神经元癫痫样放电后，ERK1/2被过度且持续激活。另外，低浓度的VPAS能在神经元癫痫样放电早期有效抑制ERK1/2的磷酸化。
The aim of the present study was to investigate the effects of valproate sodium (VPAS) on the phosphorylation extracellular signal-regulated kinase 1/2 (ERK1/2) following hippocampal neuronal epileptiform discharge in rat neurons. The study used neurons from female and male neonate Sprague-Dawley (SD) rats (at least 24 h old), which were rapidly decapitated. Following the successful development of the epileptiform discharge cell model, the neurons were divided into two groups, the VPAS group and the control group. In the concentration-response experiment, the neurons were incubated with three different concentrations of VPAS (50, 75 and 100 mg/l) 30 min prior to the epileptiform discharge. The expression of phosphorylated ERK1/2 (p-ERK1/2) was examined using an immunofluorescence technique. In the time-response experiment, the neurons were incubated with VPAS (50 mg/l) and monitored at different time-points (30 min prior to the epileptiform discharge and 0 min, 30 min, 2 h and 6 h subsequent to epileptiform discharge), and western blotting was employed to measure the changes in p-ERK1/2 protein expression. No significant differences in the expression of p-ERK1/2 among the neurons treated with different concentrations of VPAS were identified in the concentration-response experiment. However, in the time-response experiment, the expression of p-ERK1/2 30 min prior to the epileptiform discharge was significantly lower compared with that at the other time-points. Furthermore, 50 mg/l VPAS was capable of decreasing the action potential frequency of the neuronal epileptiform discharge. ERK1/2 was excessively and persistently activated following the epileptiform discharge of the neurons. In addition, a low concentration of VPAS was effective at inhibiting the phosphorylation of ERK1/2 at an earlier period of neuronal epileptiform discharge.
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乙酰胆碱通过 Ca2 /PKC/ERK1/2 信号通路诱导间充质干细胞迁移。
影响因子：
4
作者：
Tang, Jun-Ming;Yuan, Jie;Li, Qing;Wang, Jia-Ning;Kong, Xia;Zheng, Fei;Zhang, Lei;Chen, Long;Guo, Lin-Yun;Huang, Yong-Hang;Yang, Jian-Ye;Chen, Shi-You
通讯作者：
Chen, Shi-You
DOI：
10.1111/j.1749-6632.2003.tb07517.x
发表时间：
2003-01-01
期刊：
NEUROPROTECTIVE AGENTS
影响因子：
--
作者：
Bittigau, P;Sifringer, M;Ikonomidou, C
通讯作者：
Ikonomidou, C
影响因子：
7.6
作者：
Bowden, CL
通讯作者：
Bowden, CL
影响因子：
4.8
作者：
Brown MD;Sacks DB
通讯作者：
Sacks DB
影响因子：
6.1
作者：
Di Maio, Roberto;Mastroberardino, Pier G.;Greenamyre, J. Timothy
通讯作者：
Greenamyre, J. Timothy