中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2010年
19期
1348-1352
,共5页
刘庆祝%王峰%牟青春%张培松%孙涛
劉慶祝%王峰%牟青春%張培鬆%孫濤
류경축%왕봉%모청춘%장배송%손도
癫痫%岛叶%点燃%神经生长相关蛋白%突触素
癲癇%島葉%點燃%神經生長相關蛋白%突觸素
전간%도협%점연%신경생장상관단백%돌촉소
Epilepsy%Insular%Kindling%GAP-43%P38
目的 探讨神经生长相关蛋白(GAP43)和突触素(P38)基因及蛋白在岛叶电点燃致癫大鼠海马的表达及其意义.方法 健康雄性SD大鼠72只,随机分为点燃组和假手术组,每组均36只大鼠.点燃组和假手术组各随机分为1、3、7、15、30及60 d 6个亚组,每亚组大鼠6只.点然后,标本应用免疫组化、原位杂交组织化学方法研究岛叶电点燃致癫大鼠海马GAP-43及P38表达的变化.结果 致癫1 d,海马齿状同颗粒细胞、门区、CA3区锥体细胞层GAP-43mRNA及蛋白表达高于对照组(P<0.05);致癫3 d,表达减少(P>0.05),致癫7 d后,表达呈现第2次增高;15 d、30 d显著高于对照组(P<0.01);致癫60 d,仍高于对照组,但差异无统计学意义(P>0.05).P38 mRNA及蛋白表达:致癫7 d,齿状回颗粒细胞层、门区、CA3区椎体细胞杂交信号及免疫染色开始增;15 d时差异达高峰(P<0.01),这些变化一直持续到4周开始下降.结论 岛叶癫痫和颞叶海马密切相关;GAP43及P38可能是岛叶癫痫的病理基础--突触可塑性的重要分子机制.
目的 探討神經生長相關蛋白(GAP43)和突觸素(P38)基因及蛋白在島葉電點燃緻癲大鼠海馬的錶達及其意義.方法 健康雄性SD大鼠72隻,隨機分為點燃組和假手術組,每組均36隻大鼠.點燃組和假手術組各隨機分為1、3、7、15、30及60 d 6箇亞組,每亞組大鼠6隻.點然後,標本應用免疫組化、原位雜交組織化學方法研究島葉電點燃緻癲大鼠海馬GAP-43及P38錶達的變化.結果 緻癲1 d,海馬齒狀同顆粒細胞、門區、CA3區錐體細胞層GAP-43mRNA及蛋白錶達高于對照組(P<0.05);緻癲3 d,錶達減少(P>0.05),緻癲7 d後,錶達呈現第2次增高;15 d、30 d顯著高于對照組(P<0.01);緻癲60 d,仍高于對照組,但差異無統計學意義(P>0.05).P38 mRNA及蛋白錶達:緻癲7 d,齒狀迴顆粒細胞層、門區、CA3區椎體細胞雜交信號及免疫染色開始增;15 d時差異達高峰(P<0.01),這些變化一直持續到4週開始下降.結論 島葉癲癇和顳葉海馬密切相關;GAP43及P38可能是島葉癲癇的病理基礎--突觸可塑性的重要分子機製.
목적 탐토신경생장상관단백(GAP43)화돌촉소(P38)기인급단백재도협전점연치전대서해마적표체급기의의.방법 건강웅성SD대서72지,수궤분위점연조화가수술조,매조균36지대서.점연조화가수술조각수궤분위1、3、7、15、30급60 d 6개아조,매아조대서6지.점연후,표본응용면역조화、원위잡교조직화학방법연구도협전점연치전대서해마GAP-43급P38표체적변화.결과 치전1 d,해마치상동과립세포、문구、CA3구추체세포층GAP-43mRNA급단백표체고우대조조(P<0.05);치전3 d,표체감소(P>0.05),치전7 d후,표체정현제2차증고;15 d、30 d현저고우대조조(P<0.01);치전60 d,잉고우대조조,단차이무통계학의의(P>0.05).P38 mRNA급단백표체:치전7 d,치상회과립세포층、문구、CA3구추체세포잡교신호급면역염색개시증;15 d시차이체고봉(P<0.01),저사변화일직지속도4주개시하강.결론 도협전간화섭협해마밀절상관;GAP43급P38가능시도협전간적병리기출--돌촉가소성적중요분자궤제.
Objective To investigate the expression of neural growth-associated protein (GAP-43)and synaptophysin(P38)gene and protein in insular electrical kindled epileptic rats and its significance. Methods Seventy-two male adult rats were divided into kindled group ( n = 36) and sham group (n =36) randomly. Each group was further divided into 1,3, 7, 15, 30 and 60 d sub-groups (n =6) respectively.After kindling with immunohistochemical staining and hybridization in situ, the altered expressions of GAP-43 and P38 were detected in hippocampus of insular electrical kindled epilepsy rats. Results Epilepsy day 1 : GAP-43 mRNA and protein expression at hippocampus dentate gyrus granular cell layer, hilus and CA:3 pyramidal layer in the kindled group were higher than the sham group ( P < 0. 05). The expressions declined at Day 3 ( P > 0. 05 ). Expressions became elevated again at Day 7 and they were significantly higher than those in the sham group at Days 15 and 30 ( P < 0. 05 ). There was no statistical difference between two groups at Day 60 ( P > 0. 05 ). Expressions of P38 mRNA and protein:hybridization signal and immunostaining at hippocampus dentate gyrus granular cell layer, hilus and CA3 pyramidal layer began to rise at Day 7 and peaked at Day 15 ( P < 0. 01 ). They lasted 4 weeks and then began to decline. Conclusion Insular epilepsy is closely related with temporal hippocampus. GAP-43 and P38 may be the pathological basis of insular epilepsy and the key molecular mechanism of synaptie plasticity.