中华神经科杂志
中華神經科雜誌
중화신경과잡지
Chinese Journal of Neurology
2013年
9期
609-613
,共5页
汪琴%王蔚%丁新生%单春雷%乔莉%孙建国%李敏%燕兰云%沈飞飞
汪琴%王蔚%丁新生%單春雷%喬莉%孫建國%李敏%燕蘭雲%瀋飛飛
왕금%왕위%정신생%단춘뢰%교리%손건국%리민%연란운%침비비
阿尔茨海默病%淀粉样β蛋白%运动(Exercise)%神经胶质
阿爾茨海默病%澱粉樣β蛋白%運動(Exercise)%神經膠質
아이자해묵병%정분양β단백%운동(Exercise)%신경효질
Alzheimer disease%Amyloid beta-protein%Exercise%Neuroglia
目的 观察自主性运动对小鼠散发性阿尔茨海默病学习记忆损伤的早期影响及其影响途径.方法 将24只雄性C57bl/6小鼠[体重(22.5±2.5)g]采用随机数字表法完全随机分为对照组、运动对照组、模型组和治疗组,每组各6只.采用侧脑室注射β淀粉样蛋白25-35(Aβ25-35)制备散发性阿尔茨海默病模型,运动对照组和治疗组进行12 d的自主性运动,对照组和模型组不进行运动.采用Y迷宫和旷场试验分别检测小鼠短期学习记忆能力和情绪改变;HE染色观察海马CA1区神经元病理损伤情况;免疫组织化学染色检测海马区胶质炎性反应.结果 模型组较对照组小鼠短期记忆能力明显下降(进臂正确率:52.60±1.46,65.50±2.78,t =4.111,P=0.003),治疗组与模型组相比,进臂正确率有显著提升(58.57±2.17,52.60±1.46,t=-2.385,P=0.044);与对照组相比,模型组海马CA1区深染的神经细胞比例(%)明显增加(5.11±0.57,2.52±0.52,t=-4.894,P=0.003).另外,海马区星形胶质细胞活化数量以及小胶质细胞数量,治疗组与模型组相比较分别下调17.86%(与对照组比值:0.99±0.13,1.17±0.10,t=2.455,P=0.036)和26.23%(与对照组比值:0.93±0.04,1.19 ±0.11,t =2.412,P=0.043).运动对小鼠的情绪变化没有明显影响.结论 自主性运动能改善Aβ25-35小鼠海马胶质炎性反应,减轻神经细胞损伤,从而改善Aβ25-35诱导的小鼠学习记忆缺陷.
目的 觀察自主性運動對小鼠散髮性阿爾茨海默病學習記憶損傷的早期影響及其影響途徑.方法 將24隻雄性C57bl/6小鼠[體重(22.5±2.5)g]採用隨機數字錶法完全隨機分為對照組、運動對照組、模型組和治療組,每組各6隻.採用側腦室註射β澱粉樣蛋白25-35(Aβ25-35)製備散髮性阿爾茨海默病模型,運動對照組和治療組進行12 d的自主性運動,對照組和模型組不進行運動.採用Y迷宮和曠場試驗分彆檢測小鼠短期學習記憶能力和情緒改變;HE染色觀察海馬CA1區神經元病理損傷情況;免疫組織化學染色檢測海馬區膠質炎性反應.結果 模型組較對照組小鼠短期記憶能力明顯下降(進臂正確率:52.60±1.46,65.50±2.78,t =4.111,P=0.003),治療組與模型組相比,進臂正確率有顯著提升(58.57±2.17,52.60±1.46,t=-2.385,P=0.044);與對照組相比,模型組海馬CA1區深染的神經細胞比例(%)明顯增加(5.11±0.57,2.52±0.52,t=-4.894,P=0.003).另外,海馬區星形膠質細胞活化數量以及小膠質細胞數量,治療組與模型組相比較分彆下調17.86%(與對照組比值:0.99±0.13,1.17±0.10,t=2.455,P=0.036)和26.23%(與對照組比值:0.93±0.04,1.19 ±0.11,t =2.412,P=0.043).運動對小鼠的情緒變化沒有明顯影響.結論 自主性運動能改善Aβ25-35小鼠海馬膠質炎性反應,減輕神經細胞損傷,從而改善Aβ25-35誘導的小鼠學習記憶缺陷.
목적 관찰자주성운동대소서산발성아이자해묵병학습기억손상적조기영향급기영향도경.방법 장24지웅성C57bl/6소서[체중(22.5±2.5)g]채용수궤수자표법완전수궤분위대조조、운동대조조、모형조화치료조,매조각6지.채용측뇌실주사β정분양단백25-35(Aβ25-35)제비산발성아이자해묵병모형,운동대조조화치료조진행12 d적자주성운동,대조조화모형조불진행운동.채용Y미궁화광장시험분별검측소서단기학습기억능력화정서개변;HE염색관찰해마CA1구신경원병리손상정황;면역조직화학염색검측해마구효질염성반응.결과 모형조교대조조소서단기기억능력명현하강(진비정학솔:52.60±1.46,65.50±2.78,t =4.111,P=0.003),치료조여모형조상비,진비정학솔유현저제승(58.57±2.17,52.60±1.46,t=-2.385,P=0.044);여대조조상비,모형조해마CA1구심염적신경세포비례(%)명현증가(5.11±0.57,2.52±0.52,t=-4.894,P=0.003).령외,해마구성형효질세포활화수량이급소효질세포수량,치료조여모형조상비교분별하조17.86%(여대조조비치:0.99±0.13,1.17±0.10,t=2.455,P=0.036)화26.23%(여대조조비치:0.93±0.04,1.19 ±0.11,t =2.412,P=0.043).운동대소서적정서변화몰유명현영향.결론 자주성운동능개선Aβ25-35소서해마효질염성반응,감경신경세포손상,종이개선Aβ25-35유도적소서학습기억결함.
Objective To investigate the early influence and the relevant pathway of voluntary exercise against impairment of learning and memory in mice with sporadic Alzheimer' s disease.Methods Twenty-four male C57bl/6 mice (weight (22.5 ± 2.5) g) were randomly divided into 4 groups:control group,exercise control group,model group and treatment group,6 in each group.Intracerebroventricular injection of β-amyloid peptide-25-35 (Aβ25-35) was used to make mock Alzheimer' s disease,and then mice in exercise control group and treatment group were allowed to exercise training for 12 days,non-exercise to control group and model group.Y-maze and open field test were arranged to measure the short-term change of learning,memory and emotions,respectively.Neuronal damage in the hippocampal CA1 region was observed by HE staining.The expression level of glial inflammatory response was quantitatively determined with method of immunohistochemistry.Results A[25_35 could cause impairment of learning and memory (accuracy in Y maze:52.60 ± 1.46,65.50 ± 2.78,t =4.111,P =0.003; % of dark neruons in CA1 in HE staining:5.11 ± 0.57,2.52 ± 0.52,t =-4.894,P =0.003),and it could be significantly improved after exercise (accuracy in Y maze:58.57 ± 2.17,52.60 ± 1.46,t =-2.385,P =0.044).Additionally,the level of activated astrocytes and microglia expression in hippocampus decreased by 17.86% (ratio to control:0.99 ± 0.13,1.17 ± 0.10,t =2.455,P =0.036) and 26.23% (ratio to control:0.93 ± 0.04,1.19 ± 0.11,t =2.412,P =0.043),respectively.Conclusion Exercise plays an anti-inflammatory role in the progression of Alzheimer' s disease,reducing the nerve cell damage and improving learning and memory function.