锂-匹罗卡品致痫大鼠脑组织中驱动蛋白家族成员17的表达情况  

Dynamic changes of kinesin family member 17 protein expression in the pilocarpine-induced rat model

作　　者：于岫楠 周雪颖[2] 李新钢[3] 周盛年[1] 

机构地区：[1]山东大学齐鲁医院神经内科,济南250012 [2]山东中医药大学第一临床医学院 [3]山东大学齐鲁医院神经外科

出　　处：《中华神经科杂志》2013年第8期519-523,共5页Chinese Journal of Neurology

摘　　要：目的观察驱动蛋白家族成员17（KIF17）在锂一匹罗卡品致痫大鼠海马和颞叶皮质表达的变化，探讨其在癫痫发生、发展中的作用。方法采用氯化锂．匹罗卡品诱导癫痫大鼠模型，将49只雄性正常Wistar大鼠采用随机数字表法分成实验组（n=42）和对照组（n=7），实验组又分为6个亚组（n=7）：包括癫痫后24h、72h、7d、14d、1个月、2个月组。运用蛋白质印迹法检测KIFl7在致痫大鼠海马和颞叶皮质的表达变化，免疫荧光双标染色法确定KIF17的表达部位。结果大鼠海马KIF17蛋白表达在癫痫持续状态（SE）后开始增高[积分吸光度（IA）比值：24h0．516±0．196、72h0．742±0．313]，在癫痫后7d时达到高峰（0．888±0．319），之后逐渐降低（14d0．770±0．271、1个月0．742±0．261、2个月0．714±0．271），但均显著高于对照组（0．495±0．203），差异均有统计学意义（t=7．051、4．974、7．419、8．795、8．264、6．676，均P〈0．05）。大鼠颞叶皮质KIF17蛋白的表达在SE后24h时开始持续增高，并在30d时达到高峰，且L4比值均明显高于对照组。免疫荧光双标染色法显示KIF17蛋白主要存在于神经元，包括兴奋性神经元和抑制性神经元，而在星形胶质细胞中不表达。结论KIF17在锂一匹罗卡品致癫痫模型的发生发展过程中可能起着重要的作用。Objective To investigate the kinesin family member 17 （KIFI7） expression and cellular localization in the hippocampus and temporal lobe cortex in the rat lithium-piloearpine model of epilepsy, and discuss its function in the epilepsy pathogencsis. Methods The animal model was established by lithium- piloearpine induction in rats. Totally 49 adult healthy male Wistar rats were randomly divided into control group （ n = 7 ） and experimental group （ n = 42 ）. The experimental group included 6 subgroups （ n = 7 ） according to sacrifice time （24 h, 72 h, 7 d, 14 d, 1 month and 2 months）. The expression and localization of KIF17 were examined by western blot and double-label immunofluoreseenee, respectively. Results In rat hippocampus, the expression of KIF17 protein increased after the onset of seizure （the ration of KIF17/13-actin were：24 h 0. 516 ± 0. 196,72 h 0.742 ± 0. 313 ） , reached its peak in 7 days （0. 888 ±0. 319 ） and then slowed down （ 14 d 0. 770 ± 0. 271,1 month 0. 742 ±0. 261,2 months 0. 714± 0. 271 ）, all of which were significantly higher than that in the control group （ 0. 495 ±0. 203 ）. And all the differences had statistical significance （t =7. 051,4. 974,7. 419,8. 795,8. 264,6. 676, all P 〈0. 05）. In rat cortex of temporal lobe, the expression of KIF17 protein increased after the onset of seizure and reached its peak in 30 d. The optical density ration in the experimental groups were higher than that in the control group. Double- label immunofluorescence disclosed that the KIF17 localized in the neurons, including excitable neurons and inhibitory neurons, but not in the astroeytes which were performed with anti-mierotubule-assoeiated protein 2, anti-brain-specific Na-dependent inorganic phosphate cotransporter, anti-glutamate deearboxylase 1 and anti-glial fibrillary acidic protein, respectively. Conclusion KIF17 may play a potential role in the pathogenetie mechanisms of the rat lithium-piloearpine model of epilepsy.

关 键 词：癫痫 颞叶 驱动蛋白 毛果芸香碱 疾病模型 动物 

分 类 号：R971.6[医药卫生—药品]