中国临床康复
中國臨床康複
중국림상강복
CHINESE JOURNAL OF CLINICAL REHABILITATION
2004年
25期
5444-5445
,共2页
章茜%程江涛%杨春%王书春%王一菱%吴景兰%王雨若
章茜%程江濤%楊春%王書春%王一蔆%吳景蘭%王雨若
장천%정강도%양춘%왕서춘%왕일릉%오경란%왕우약
睡眠剥夺%海马/病理学%神经元/病理学%基因表达
睡眠剝奪%海馬/病理學%神經元/病理學%基因錶達
수면박탈%해마/병이학%신경원/병이학%기인표체
背景:睡眠剥夺是否引起细胞变性,其信号传导是否与某些基因调控有关.目的:探讨睡眠剥夺引起的神经元凋亡与相关基因表达的变化.设计:随机对照实验研究.地点和材料:实验地点:郑州大学医学院生理学实验室.成年健康SD大鼠,雌雄不限,体质量(200±20)g,由河南省实验动物中心提供.干预:采用TUNEL染色观察了快眼动睡眠剥夺大鼠海马神经元形态学变化,应用原位杂交检测了快眼动睡眠剥夺大鼠海马bcl-2,bax mRNA表达.主要观察指标:睡眠剥夺大鼠海马神经元形态学变化;海马bcl-2和baxmRNA表达.结果:快眼动睡眠剥夺大鼠海马CA1,CA3区神经元阳性凋亡细胞数增多,异相睡眠剥夺组海马CA1~CA4区细胞凋亡率分别为(6.60±2.24)%,(1.69±0.45)%,(6.87±1.32)%,(1.74±0.98)%.CAl,CA3区细胞凋亡率和CA2,CA4区相比较差异有显著性意义(t=5.26~6.95,P<0.05).bcl-2 mRNA阳性信号表达积分值较强,四个区之间差异无显著性意义,bax mRNA表达增强[CA1为(211.12±59.85);CA3为(205.56±56.99)]与CA2和CA4区[(123.42±22.80),(124.21±20.47)]比较差异有显著性意义(t=3.20~4.36,P<0.05).结论:睡眠剥夺可引起大鼠海马神经元凋亡,与凋亡相关的bcl-2,baxmRNA基因表达的变化可能涉及神经元的凋亡机制.
揹景:睡眠剝奪是否引起細胞變性,其信號傳導是否與某些基因調控有關.目的:探討睡眠剝奪引起的神經元凋亡與相關基因錶達的變化.設計:隨機對照實驗研究.地點和材料:實驗地點:鄭州大學醫學院生理學實驗室.成年健康SD大鼠,雌雄不限,體質量(200±20)g,由河南省實驗動物中心提供.榦預:採用TUNEL染色觀察瞭快眼動睡眠剝奪大鼠海馬神經元形態學變化,應用原位雜交檢測瞭快眼動睡眠剝奪大鼠海馬bcl-2,bax mRNA錶達.主要觀察指標:睡眠剝奪大鼠海馬神經元形態學變化;海馬bcl-2和baxmRNA錶達.結果:快眼動睡眠剝奪大鼠海馬CA1,CA3區神經元暘性凋亡細胞數增多,異相睡眠剝奪組海馬CA1~CA4區細胞凋亡率分彆為(6.60±2.24)%,(1.69±0.45)%,(6.87±1.32)%,(1.74±0.98)%.CAl,CA3區細胞凋亡率和CA2,CA4區相比較差異有顯著性意義(t=5.26~6.95,P<0.05).bcl-2 mRNA暘性信號錶達積分值較彊,四箇區之間差異無顯著性意義,bax mRNA錶達增彊[CA1為(211.12±59.85);CA3為(205.56±56.99)]與CA2和CA4區[(123.42±22.80),(124.21±20.47)]比較差異有顯著性意義(t=3.20~4.36,P<0.05).結論:睡眠剝奪可引起大鼠海馬神經元凋亡,與凋亡相關的bcl-2,baxmRNA基因錶達的變化可能涉及神經元的凋亡機製.
배경:수면박탈시부인기세포변성,기신호전도시부여모사기인조공유관.목적:탐토수면박탈인기적신경원조망여상관기인표체적변화.설계:수궤대조실험연구.지점화재료:실험지점:정주대학의학원생이학실험실.성년건강SD대서,자웅불한,체질량(200±20)g,유하남성실험동물중심제공.간예:채용TUNEL염색관찰료쾌안동수면박탈대서해마신경원형태학변화,응용원위잡교검측료쾌안동수면박탈대서해마bcl-2,bax mRNA표체.주요관찰지표:수면박탈대서해마신경원형태학변화;해마bcl-2화baxmRNA표체.결과:쾌안동수면박탈대서해마CA1,CA3구신경원양성조망세포수증다,이상수면박탈조해마CA1~CA4구세포조망솔분별위(6.60±2.24)%,(1.69±0.45)%,(6.87±1.32)%,(1.74±0.98)%.CAl,CA3구세포조망솔화CA2,CA4구상비교차이유현저성의의(t=5.26~6.95,P<0.05).bcl-2 mRNA양성신호표체적분치교강,사개구지간차이무현저성의의,bax mRNA표체증강[CA1위(211.12±59.85);CA3위(205.56±56.99)]여CA2화CA4구[(123.42±22.80),(124.21±20.47)]비교차이유현저성의의(t=3.20~4.36,P<0.05).결론:수면박탈가인기대서해마신경원조망,여조망상관적bcl-2,baxmRNA기인표체적변화가능섭급신경원적조망궤제.
BACKGROUND: To make sure whether sleep deprivation will cause cell degeneration and if its signal conduction is related to expressions of certain genes.OBJECTIVE: To explore the apoptosis of neutrons caused by sleep deprivation as well as the expressive changes of related genes.DESIGN: Randomized case controlled study.SETTING and MATERIALS: Experimental site: Physiological Laboratory of School of Medicine, Zhengzhou University. Adult SD rats provided by Experimental Animal Center of Henan Province which weighed about (200 ± 20) g were chosen of either sex.INTERVENTIONS: TUNEL dyeing method was used to observe the morphologic changes of neurons in hippocampus of rats caused by rapid eye movement sleep deprivation. The expressions of mRNA of bcl-2 and bax in hippocampus of rats were detected by in situ hybridization.MAIN OUTCOME MEASURES: The morphologic changes of neurons in hippocampus of rats caused by sleep deprivation; expressions of mRNA of bcl-2 and bax in hippocampus.RESULTS: The number of positive apoptosis neurons in CA1, CA3 regions of hippocampus in rats was increased after rapid eye movement sleep deprivation. The apoptosis rates of cells in CA1 to CA4 regions in hippocampus caused by paradoxical sleep deprivation were(6.60 ±2.24)% ,(1.69 ±0. 45)% , (6. 87 ± 1.32)% and (1.74 ±0. 98)% respectively.There was significant difference between the apoptosis rates of CA1, CA3 regions and CA2, CA4 regions( t =5.26 -6.95, P <0. 05). The value of positive signal expressions of bcl-2 mRNA was much stronger without different between four regions. The expression of bax mRNA was increased, there was difference between the expressions of CA1(211.12 ±59. 85), CA3(205.56 ±56.99)and CA2 ( 123.42 ± 22.80), CA4 ( 124. 21 ± 20.47 ) ( t = 3.20 - 4.36,P < 0.05).CONCLUSION: Sleep deprivation can lead to neuronal apoptosis in hippocampus of rats. The expressive changes of mRNA of bcl-2 and bax may be the mechanism of neuron apoptosis.