中华神经科杂志
中華神經科雜誌
중화신경과잡지
Chinese Journal of Neurology
2013年
8期
519-523
,共5页
于岫楠%周雪颖%李新钢%周盛年
于岫楠%週雪穎%李新鋼%週盛年
우수남%주설영%리신강%주성년
癫痫,颞叶%驱动蛋白%毛果芸香碱%疾病模型,动物
癲癇,顳葉%驅動蛋白%毛果蕓香堿%疾病模型,動物
전간,섭협%구동단백%모과예향감%질병모형,동물
Epilepsy,temporal lobe%Kinesin%Pilocarpine%Disease models,animal
目的 观察驱动蛋白家族成员17 (KIF17)在锂-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、72 h、7d、14 d、1个月、2个月组.运用蛋白质印迹法检测KIF17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(L4)比值:24 h 0.516±0.196、72 h0.742±0.313],在癫痫后7d时达到高峰(0.888±0.319),之后逐渐降低(14 d 0.770±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30 d时达到高峰,且IA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-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.
目的 觀察驅動蛋白傢族成員17 (KIF17)在鋰-匹囉卡品緻癇大鼠海馬和顳葉皮質錶達的變化,探討其在癲癇髮生、髮展中的作用.方法 採用氯化鋰-匹囉卡品誘導癲癇大鼠模型,將49隻雄性正常Wistar大鼠採用隨機數字錶法分成實驗組(n=42)和對照組(n=7),實驗組又分為6箇亞組(n=7):包括癲癇後24h、72 h、7d、14 d、1箇月、2箇月組.運用蛋白質印跡法檢測KIF17在緻癇大鼠海馬和顳葉皮質的錶達變化,免疫熒光雙標染色法確定KIF17的錶達部位.結果 大鼠海馬KIF17蛋白錶達在癲癇持續狀態(SE)後開始增高[積分吸光度(L4)比值:24 h 0.516±0.196、72 h0.742±0.313],在癲癇後7d時達到高峰(0.888±0.319),之後逐漸降低(14 d 0.770±0.271、1箇月0.742±0.261、2箇月0.714±0.271),但均顯著高于對照組(0.495±0.203),差異均有統計學意義(t=7.051、4.974、7.419、8.795、8.264、6.676,均P＜0.05).大鼠顳葉皮質KIF17蛋白的錶達在SE後24h時開始持續增高,併在30 d時達到高峰,且IA比值均明顯高于對照組.免疫熒光雙標染色法顯示KIF17蛋白主要存在于神經元,包括興奮性神經元和抑製性神經元,而在星形膠質細胞中不錶達.結論 KIF17在鋰-匹囉卡品緻癲癇模型的髮生髮展過程中可能起著重要的作用.
목적 관찰구동단백가족성원17 (KIF17)재리-필라잡품치간대서해마화섭협피질표체적변화,탐토기재전간발생、발전중적작용.방법 채용록화리-필라잡품유도전간대서모형,장49지웅성정상Wistar대서채용수궤수자표법분성실험조(n=42)화대조조(n=7),실험조우분위6개아조(n=7):포괄전간후24h、72 h、7d、14 d、1개월、2개월조.운용단백질인적법검측KIF17재치간대서해마화섭협피질적표체변화,면역형광쌍표염색법학정KIF17적표체부위.결과 대서해마KIF17단백표체재전간지속상태(SE)후개시증고[적분흡광도(L4)비치:24 h 0.516±0.196、72 h0.742±0.313],재전간후7d시체도고봉(0.888±0.319),지후축점강저(14 d 0.770±0.271、1개월0.742±0.261、2개월0.714±0.271),단균현저고우대조조(0.495±0.203),차이균유통계학의의(t=7.051、4.974、7.419、8.795、8.264、6.676,균P＜0.05).대서섭협피질KIF17단백적표체재SE후24h시개시지속증고,병재30 d시체도고봉,차IA비치균명현고우대조조.면역형광쌍표염색법현시KIF17단백주요존재우신경원,포괄흥강성신경원화억제성신경원,이재성형효질세포중불표체.결론 KIF17재리-필라잡품치전간모형적발생발전과정중가능기착중요적작용.
Objective To investigate the kinesin family member 17 (KIF17) expression and cellular localization in the hippocampus and temporal lobe cortex in the rat lithium-pilocarpine model of epilepsy,and discuss its function in the epilepsy pathogenesis.Methods The animal model was established by lithiumpilocarpine 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 immunofluorescence,respectively.Results In rat hippocampus,the expression of KIF17 protein increased after the onset of seizure (the ration of KIF17/β-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.Doublelabel immunofluorescence disclosed that the KIF17 localized in the neurons,including excitable neurons and inhibitory neurons,but not in the astrocytes which were performed with anti-microtubule-associated protein 2,anti-brain-specific Na-dependent inorganic phosphate cotransporter,anti-glutamate decarboxylase 1 and anti-glial fibrillary acidic protein,respectively.Conclusion KIF17 may play a potential role in the pathogenetic mechanisms of the rat lithium-pilocarpine model of epilepsy.
