中华行为医学与脑科学杂志
中華行為醫學與腦科學雜誌
중화행위의학여뇌과학잡지
CHINESE JOURNAL OF BEHAVIORAL MEDICINE AND BRAIN SCIENCE
2013年
8期
696-699
,共4页
孔庆霞%梁汝庆%高建英%孙冉%李雷%褚旭%夏敏
孔慶霞%樑汝慶%高建英%孫冉%李雷%褚旭%夏敏
공경하%량여경%고건영%손염%리뢰%저욱%하민
癫痫%神经细胞黏附分子1%细胞外信号调节激酶2%认知功能障碍
癲癇%神經細胞黏附分子1%細胞外信號調節激酶2%認知功能障礙
전간%신경세포점부분자1%세포외신호조절격매2%인지공능장애
Epilepsy%NCAM1%ERK2%Cognitive dysfunction
目的 探讨细胞外信号调节激酶2(ERK2)及神经细胞黏附分子1(NCAM1)在癫痫认知功能障碍中的作用及抗痫、促智药物对二者作用.方法 将120只Wistar大鼠分为对照组、致痫组和卡马西平组、奥卡西平组、茴拉西坦组、盐酸多奈哌齐组治疗30 d,对照组用生理盐水造模,其余5组用匹罗卡品诱导癫痫模型,将造模成功的大鼠给予上述成药物干预模型,大鼠的学习记忆能力通过Morris水迷宫实验测试,记录逃避潜伏期和原平台象限游泳时间；并用RT-PCR法检测NCAM1、ERK2在大鼠海马组织中的mRNA表达,免疫组化法检测大鼠海马组织中NCAM1和ERK2的蛋白表达.结果 定位航行试验中,与对照组大鼠逃避潜伏期相比,致痫组[(67.14±7.37)s]＞对照组[(35.78±4.84)s](P＜0.01),其中卡马西平组与盐酸多奈哌齐组与致痫组比较,卡马西平组[(81.23±9.46)s]＞致痫组[(67.14±7.37)s](P＜0.01),盐酸多奈哌齐组[(53.75±6.74)s]＜致痫组[(67.14±7.37)s](P＜0.01).各组ERK2蛋白表达及mRNA比较为:卡马西平组＜奥卡西平组＜致痫组＜茴拉西坦组＜多奈哌齐组＜对照组.与对照组比,多奈哌齐组＞对照组(P＜0.01),茴拉西坦组＞对照组(P＜0.05).结论 ERK2在癫痫发作30 d时在海马的表达水平下降,NCAM1则相反,ERK2活性的减低和NCAM1的过度表达可能是癫痫后认知功能损害的潜在机制.卡马西平能加重癫痫认知功能障碍程度,盐酸多奈哌齐可明显改善癫痫鼠的认知功能.
目的 探討細胞外信號調節激酶2(ERK2)及神經細胞黏附分子1(NCAM1)在癲癇認知功能障礙中的作用及抗癇、促智藥物對二者作用.方法 將120隻Wistar大鼠分為對照組、緻癇組和卡馬西平組、奧卡西平組、茴拉西坦組、鹽痠多奈哌齊組治療30 d,對照組用生理鹽水造模,其餘5組用匹囉卡品誘導癲癇模型,將造模成功的大鼠給予上述成藥物榦預模型,大鼠的學習記憶能力通過Morris水迷宮實驗測試,記錄逃避潛伏期和原平檯象限遊泳時間；併用RT-PCR法檢測NCAM1、ERK2在大鼠海馬組織中的mRNA錶達,免疫組化法檢測大鼠海馬組織中NCAM1和ERK2的蛋白錶達.結果 定位航行試驗中,與對照組大鼠逃避潛伏期相比,緻癇組[(67.14±7.37)s]＞對照組[(35.78±4.84)s](P＜0.01),其中卡馬西平組與鹽痠多奈哌齊組與緻癇組比較,卡馬西平組[(81.23±9.46)s]＞緻癇組[(67.14±7.37)s](P＜0.01),鹽痠多奈哌齊組[(53.75±6.74)s]＜緻癇組[(67.14±7.37)s](P＜0.01).各組ERK2蛋白錶達及mRNA比較為:卡馬西平組＜奧卡西平組＜緻癇組＜茴拉西坦組＜多奈哌齊組＜對照組.與對照組比,多奈哌齊組＞對照組(P＜0.01),茴拉西坦組＞對照組(P＜0.05).結論 ERK2在癲癇髮作30 d時在海馬的錶達水平下降,NCAM1則相反,ERK2活性的減低和NCAM1的過度錶達可能是癲癇後認知功能損害的潛在機製.卡馬西平能加重癲癇認知功能障礙程度,鹽痠多奈哌齊可明顯改善癲癇鼠的認知功能.
목적 탐토세포외신호조절격매2(ERK2)급신경세포점부분자1(NCAM1)재전간인지공능장애중적작용급항간、촉지약물대이자작용.방법 장120지Wistar대서분위대조조、치간조화잡마서평조、오잡서평조、회랍서탄조、염산다내고제조치료30 d,대조조용생리염수조모,기여5조용필라잡품유도전간모형,장조모성공적대서급여상술성약물간예모형,대서적학습기억능력통과Morris수미궁실험측시,기록도피잠복기화원평태상한유영시간；병용RT-PCR법검측NCAM1、ERK2재대서해마조직중적mRNA표체,면역조화법검측대서해마조직중NCAM1화ERK2적단백표체.결과 정위항행시험중,여대조조대서도피잠복기상비,치간조[(67.14±7.37)s]＞대조조[(35.78±4.84)s](P＜0.01),기중잡마서평조여염산다내고제조여치간조비교,잡마서평조[(81.23±9.46)s]＞치간조[(67.14±7.37)s](P＜0.01),염산다내고제조[(53.75±6.74)s]＜치간조[(67.14±7.37)s](P＜0.01).각조ERK2단백표체급mRNA비교위:잡마서평조＜오잡서평조＜치간조＜회랍서탄조＜다내고제조＜대조조.여대조조비,다내고제조＞대조조(P＜0.01),회랍서탄조＞대조조(P＜0.05).결론 ERK2재전간발작30 d시재해마적표체수평하강,NCAM1칙상반,ERK2활성적감저화NCAM1적과도표체가능시전간후인지공능손해적잠재궤제.잡마서평능가중전간인지공능장애정도,염산다내고제가명현개선전간서적인지공능.
Objective To study the effect of anti-epileptic,nootropic drugs on the expression of NCAM and ERK2 in the hippocampus changes on the epileptic rats with cognitive dysfunction.Methods A total of 120Wistar rats were used.20 controls and 100 in which epilepticus with cognitive dysfunction were randomly assigned to 5 groups (n =20/group) that received daily treatments for 30 days with either (1) saline (epilepsy),(2) carbamazine (traditional anti-epileptic),(3) oxcarbazine (new anti-epileptic),(4) aniracetam (brain protective),or (5) donepezil (nootopic).Spatial learning and memory were assessed with a Morris Water Maze (MWM).Hippocampus tissue was assessed for NCAM1 and ERK-2 mRNAs by RT-PCR and proteins by immunochemistry.Results The mean escape latency of the place navigation test:EP group ((67.14 ± 7.37)s)was all higher than NS group (35.78 ± 4.84 s)and there was statistical significance (P ＜ 0.01),carbamazepine group ((81.23 ± 9.46)s) ＞ EP group((67.14 ±7.37)s) ＞ donepezi group((53.75 ±6.74) s) (P＜0.01).Immunohistochemical and RT-PCR result:carbamazepine ＜ oxcarbazepine ＜ epilepsy ＜ aniracetam ＜ donepezi group.Compared with control group,donepezil group ＞ control group (P ＜ 0.01),aniracetam group ＞ control group (P ＜ 0.05).Conclusion ERK-2 expression is decreased and NCAM 1 expression is increased in the hippocampus in the epileptic rats.Thus,both are involved in cognitive dysfunction.Carbamazepine aggravates cognitive dysfunction,whereas donepezil improves cognitive dysfunction associated with epilepsy.
