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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。
Objective To investigate the role of CDK inhibitors in epileptic seizures induced by Licl-Pilocarpine-induced temporal lobe epilepsy in rats and its related mechanisms. Methods Interliver temporal lobe epilepsy model was made with Licl-Pilocarpine. Olomoucine, a CDK inhibitor, was intervened on the 3rd, 4th, 5th day after the persistence of epilepsy in rats. The rats were divided into normal group, model Group, intervention group and control group. Video interception of epilepsy in each group was recorded. The latency from the first chronic spontaneous seizure, the frequency of chronic spontaneous seizure and the mortality of the rats throughout the whole process were recorded EEG was used to monitor the changes of electroencephalogram in chronic spontaneous seizure rats in each group, and the distribution of spikes was recorded during the seizure. GFAP (glial fibrillary acidic protein, A marker of stromal cells) and ADK (adenosine kinase). Results Compared with the model group, the latency of the first attack was significantly prolonged and the frequency of clinical attack was significantly decreased (P <0.05). The expression of GFAP and ADK was significantly decreased (P <0.05) ). The expression of GFAP and ADK in the model group was significantly higher than that in the normal group. There was no significant change in the control group compared with the model group. Conclusions CDK inhibitors can reduce the number of epileptic seizures and the spike wave distribution of epilepsy in rats to a certain extent. The mechanism may be that cell cycle-dependent kinase inhibitors can inhibit astrocyte proliferation and reduce ADK Of the expression, an indirect increase in endogenous epileptic agent adenosine content.