中华神经医学杂志
中華神經醫學雜誌
중화신경의학잡지
CHINESE JOURNAL OF NEUROMEDICINE
2013年
8期
774-778
,共5页
孔庆霞%王种%李雷%梁汝庆%孙冉%夏敏%褚旭
孔慶霞%王種%李雷%樑汝慶%孫冉%夏敏%褚旭
공경하%왕충%리뢰%량여경%손염%하민%저욱
癫痫%神经细胞黏附分子1%认知功能障碍
癲癇%神經細胞黏附分子1%認知功能障礙
전간%신경세포점부분자1%인지공능장애
Epilepsy%Neural cell adhesion molecule 1%Cognitive dysfunction
目的 研究神经细胞黏附分子1(NCAMl)与癫痫大鼠认知功能障碍发病机制之间的相关性,探讨其在癫痫认知功能障碍中发挥的作用. 方法 采用随机数字表法将120只Wistar大鼠分为实验组和对照组.实验组又分为致痫组、卡马西平治疗组、奥卡西平治疗组、茴拉西坦治疗组、盐酸多奈哌齐治疗组,每组20只;采用匹罗卡品诱导癫痫模型,后4组并灌服相应药物.对照组(n=20)不造模,灌服生理盐水造模.通过Morris水迷宫实验测试大鼠的学习记忆能力,并通过RT-PCR法检测大鼠海马组织中NCAM1 mRNA表达,免疫组化法检测大鼠海马组织中NCAM1蛋白表达. 结果 各组大鼠水迷宫实验逃逸潜伏期差异有统计学意义(F=91.920,P=0.000),按长短排序为:卡马西平组>奥卡西平组>茴拉西坦组>致痫组>盐酸多奈哌齐组>对照组.各组大鼠免疫组化及RT-PCR结果差异亦有统计学意义(F=324.510,P=0.000; F=81.160,P=0.000),按表达量多少排序为:盐酸多奈哌齐组>茴拉西坦组>致痫组>奥卡西平组>卡马西平组>对照组. 结论 癫痫发作30d后海马的NCAM1表达水平升高,参与了癫痫认知功能障碍的发病;抗癫痫药物能加重癫痫认知功能障碍的发生,促智药物可明显改善癫痫的认知功能.
目的 研究神經細胞黏附分子1(NCAMl)與癲癇大鼠認知功能障礙髮病機製之間的相關性,探討其在癲癇認知功能障礙中髮揮的作用. 方法 採用隨機數字錶法將120隻Wistar大鼠分為實驗組和對照組.實驗組又分為緻癇組、卡馬西平治療組、奧卡西平治療組、茴拉西坦治療組、鹽痠多奈哌齊治療組,每組20隻;採用匹囉卡品誘導癲癇模型,後4組併灌服相應藥物.對照組(n=20)不造模,灌服生理鹽水造模.通過Morris水迷宮實驗測試大鼠的學習記憶能力,併通過RT-PCR法檢測大鼠海馬組織中NCAM1 mRNA錶達,免疫組化法檢測大鼠海馬組織中NCAM1蛋白錶達. 結果 各組大鼠水迷宮實驗逃逸潛伏期差異有統計學意義(F=91.920,P=0.000),按長短排序為:卡馬西平組>奧卡西平組>茴拉西坦組>緻癇組>鹽痠多奈哌齊組>對照組.各組大鼠免疫組化及RT-PCR結果差異亦有統計學意義(F=324.510,P=0.000; F=81.160,P=0.000),按錶達量多少排序為:鹽痠多奈哌齊組>茴拉西坦組>緻癇組>奧卡西平組>卡馬西平組>對照組. 結論 癲癇髮作30d後海馬的NCAM1錶達水平升高,參與瞭癲癇認知功能障礙的髮病;抗癲癇藥物能加重癲癇認知功能障礙的髮生,促智藥物可明顯改善癲癇的認知功能.
목적 연구신경세포점부분자1(NCAMl)여전간대서인지공능장애발병궤제지간적상관성,탐토기재전간인지공능장애중발휘적작용. 방법 채용수궤수자표법장120지Wistar대서분위실험조화대조조.실험조우분위치간조、잡마서평치료조、오잡서평치료조、회랍서탄치료조、염산다내고제치료조,매조20지;채용필라잡품유도전간모형,후4조병관복상응약물.대조조(n=20)불조모,관복생리염수조모.통과Morris수미궁실험측시대서적학습기억능력,병통과RT-PCR법검측대서해마조직중NCAM1 mRNA표체,면역조화법검측대서해마조직중NCAM1단백표체. 결과 각조대서수미궁실험도일잠복기차이유통계학의의(F=91.920,P=0.000),안장단배서위:잡마서평조>오잡서평조>회랍서탄조>치간조>염산다내고제조>대조조.각조대서면역조화급RT-PCR결과차이역유통계학의의(F=324.510,P=0.000; F=81.160,P=0.000),안표체량다소배서위:염산다내고제조>회랍서탄조>치간조>오잡서평조>잡마서평조>대조조. 결론 전간발작30d후해마적NCAM1표체수평승고,삼여료전간인지공능장애적발병;항전간약물능가중전간인지공능장애적발생,촉지약물가명현개선전간적인지공능.
Objective To study the correlation of neural cell adhesion molecule 1 (NCAM1) with pathogenesis of cognitive dysfunction in epileptic rats and explore its effect on cognitive dysfunction in epileptic rats.Methods A total of 120 Wistar rats were randomly assigned to control group (n=20) and experimental group (n=100); and rats in the experimental group were subdivided into 5 groups (n=20),the epilepsy models were induced by pilocarpine,and rats in these 5 groups received daily treatments for 30 days with either saline,carbamazine,oxcarbazine,aniracetam or donepezil (nootopic).Spatial learning and memory abilities were assessed with Water Maze test.Hippocampus tissue was assessed for NCAM1 mRNAs by RT-PCR and proteins by immunochemistry.Results The mean escape latency of rats in the Morris water maze test:carbamazepine treatment group >oxcarbazepine treatment group >aniracetam treatment group >epilepsy group >donepezi treatment group; significant differences were noted between each two groups (F=91.920,P=0.000).Immunohistochemical and RT-PCR results:donepezi treatment rgroup >aniracetam treatment group >epileptic group >oxcarbazepine treatment group >carbamazepine treatment group> control group; there were differences between each 2 groups (Immunohistochemical result:F=324.510,P=0.000; RT-PCR result:F=81.160,P=0.000).Conclusion NCAM1 expression in the hippocampus rises within 30 days of epileptic attack,who participates in the pathogenesis of cognitive dysfunction; carbamazepine can aggravate the cognitive dysfunction and donepezil can obviously improve the cognitive function of epilepsy.