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Increased expression of Notch1 in temporal lobe epilepsy: animal models and clinical evidence 被引量:1
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作者 Xijin Liu Zhiyong Yang +1 位作者 Yaping Yin Xuejun Deng 《Neural Regeneration Research》 SCIE CAS CSCD 2014年第5期526-533,共8页
Temporal lobe epilepsy is associated with astrogliosis. Notchl signaling can induce astrogliosis in glioma. However, it remains unknown whether Notchl signaling is involved in the pathogenesis of epilepsy. This study ... Temporal lobe epilepsy is associated with astrogliosis. Notchl signaling can induce astrogliosis in glioma. However, it remains unknown whether Notchl signaling is involved in the pathogenesis of epilepsy. This study investigated the presence of Notchl, hairy and enhancer of split-l, and glial fibrillary acidic protein in the temporal neocortex and hippocampus of lithium-pilocar- pine-treated rats. The presence of Notchl and hairy and enhancer of split-1 was also explored in brain tissues of patients with intractable temporal lobe epilepsy. Quantitative electroencephalo- gram analysis and behavioral observations were used as auxiliary measures. Results revealed that the presence of Notchl, hairy and enhancer of split-l, and glial fibriUary acidic protein were en- hanced in status epilepticus and vehicle-treated spontaneous recurrent seizures rats, but remain unchanged in the following groups: control, absence of either status epilepticus or spontaneous recurrent seizures, and zileuton-treated spontaneous recurrent seizures. Compared with patient control cases, the presences of Notch1 and hairy and enhancer of split- 1 were upregulated in the temporal neocortex of patients with intractable temporal lobe epilepsy. Therefore, these results suggest that Notchl signaling may play an important role in the onset of temporal lobe epilepsy via astrogliosis. Furthermore, zileuton may be a potential therapeutic strategy for temporal lobe epilepsy by blocking Notchl signaling. 展开更多
关键词 nerve regeneration brain injury epilepsy temporal lobe epilepsy ASTROGLIOSIS Notch 1 hairy and enhancer of split-1 glial fibrillary acidic protein licl-pilocarpine ZILEUTON the Natural Science Foundation of Hubei Province neural regeneration
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Olomoucine在匹罗卡品所致颞叶癫痫间中的作用及机制的研究
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作者 殷亚萍 刘希金 +1 位作者 杨志勇 邓学军 《卒中与神经疾病》 2013年第4期195-199,共5页
目的研究细胞周期依赖激酶(CDK)抑制剂在氯化锂-匹罗卡品(Licl-Pilocarpine)所致颞叶癫痫间大鼠痫间性发作中的作用及其相关机制。方法用Licl-Pilocarpine制作大鼠颞叶癫痫间模型;用CDK抑制剂Olomoucine在大鼠癫痫间持续状态后第3、4、... 目的研究细胞周期依赖激酶(CDK)抑制剂在氯化锂-匹罗卡品(Licl-Pilocarpine)所致颞叶癫痫间大鼠痫间性发作中的作用及其相关机制。方法用Licl-Pilocarpine制作大鼠颞叶癫痫间模型;用CDK抑制剂Olomoucine在大鼠癫痫间持续状态后第3、4、5 d进行干预,并将参与实验的大鼠分为正常组、模型组、干预组和对照组;用视频监测各组大鼠的癫痫间发作情况,记录距离第1次慢性自发性发作的潜伏期、慢性自发性发作的频率及贯穿于整个过程中大鼠的病死率;用脑电图监测各组出现慢性自发性发作大鼠的脑电活动的变化,记录发作间期棘波发放的情况;用免疫组化检测GFAP(胶质纤维酸性蛋白,一种星形胶质细胞的标记物)和ADK(腺苷激酶)的表达水平。结果干预组较模型组距第1次发作的潜伏期明显延长,临床发作次数明显减少,棘波发作的频率和持续时间明显缩短(P<0.05);GFAP和ADK的表达量明显下降(P<0.05);模型组较正常组GFAP和ADK的表达量明显增加;对照组较模型组无明显变化。结论 CDK抑制剂在一定程度上能够减少癫痫间大鼠的痫间性发作次数和脑电波的棘波发放,其机制可能为细胞周期依赖激酶抑制剂能够抑制星形胶质细胞的增生,减少ADK的表达,间接的增加了内源性止痫间剂腺苷的含量。 展开更多
关键词 licl-pilocarpine 颞叶癫痫间 CDK OLOMOUCINE 胶质细胞增生
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