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
2009年
12期
1064-1066
,共3页
高宝兵%龙志敏%贺桂琼%孙善全
高寶兵%龍誌敏%賀桂瓊%孫善全
고보병%룡지민%하계경%손선전
常压高氧%阿尔茨海默病%学习记忆%β-淀粉样蛋白
常壓高氧%阿爾茨海默病%學習記憶%β-澱粉樣蛋白
상압고양%아이자해묵병%학습기억%β-정분양단백
Normobaric hyperoxia%Alzheimer's disease%Learning and memory%Aβ amyloid
目的 探讨常压高氧(NH)处理是否改善APP/PS1双重转基因AD模型小鼠的空间学习和记忆能力.方法 对APP/PS1双重转基因AD模型种鼠交配后产下的子代小鼠进行基因分型,待子代达10周时,取双重转基因小鼠20只,随机分成A、B2组(每组10只).A组小鼠给予常压高氧(40%O_2, 60%空气)处理,8h/d,持续8周;B组常规喂养,作为对照.高氧处理后进行Morris水迷宫实验,分别检测各组小鼠在可视平台、隐蔽平台及空间探索实验中找到平台的时间及搜索的平均路程;行为学实验结束后,采用ELISA定量检测小鼠脑内Aβ水平.结果 行为学实验结果:(1)可视平台下,2组小鼠找到平台的时间及搜索的平均路程差异尤显著性(P>0.05);(2)隐蔽平台下,高氧处理组小鼠找到平台的时间及搜索的平均路程较对照组明显缩短(P<0.01);(3)空间探索实验中,高氧处理组小鼠经过平台的次数[(6.31±2.55)次]显著高丁对照组[(3.13±1.59)7欠](P<0.01).ELISA结果显示,高氧处理组小鼠大脑皮质及海马内Aβ40[(783.64±97.21)pg/ml和Aβ42(175.30±17.09)pg/ml]水平显著低于对照组[Aβ40(1251.59±42.29)pg/ml、Aβ42(286.83±12.96)pg/ml](P<0.01).结论 常压高氧处理能显著改善AD模型小鼠空间学习记忆障碍;常压高氧可能通过减少Aβ生成或/和促进血管内皮细胞清除Aβ而发挥作用.
目的 探討常壓高氧(NH)處理是否改善APP/PS1雙重轉基因AD模型小鼠的空間學習和記憶能力.方法 對APP/PS1雙重轉基因AD模型種鼠交配後產下的子代小鼠進行基因分型,待子代達10週時,取雙重轉基因小鼠20隻,隨機分成A、B2組(每組10隻).A組小鼠給予常壓高氧(40%O_2, 60%空氣)處理,8h/d,持續8週;B組常規餵養,作為對照.高氧處理後進行Morris水迷宮實驗,分彆檢測各組小鼠在可視平檯、隱蔽平檯及空間探索實驗中找到平檯的時間及搜索的平均路程;行為學實驗結束後,採用ELISA定量檢測小鼠腦內Aβ水平.結果 行為學實驗結果:(1)可視平檯下,2組小鼠找到平檯的時間及搜索的平均路程差異尤顯著性(P>0.05);(2)隱蔽平檯下,高氧處理組小鼠找到平檯的時間及搜索的平均路程較對照組明顯縮短(P<0.01);(3)空間探索實驗中,高氧處理組小鼠經過平檯的次數[(6.31±2.55)次]顯著高丁對照組[(3.13±1.59)7欠](P<0.01).ELISA結果顯示,高氧處理組小鼠大腦皮質及海馬內Aβ40[(783.64±97.21)pg/ml和Aβ42(175.30±17.09)pg/ml]水平顯著低于對照組[Aβ40(1251.59±42.29)pg/ml、Aβ42(286.83±12.96)pg/ml](P<0.01).結論 常壓高氧處理能顯著改善AD模型小鼠空間學習記憶障礙;常壓高氧可能通過減少Aβ生成或/和促進血管內皮細胞清除Aβ而髮揮作用.
목적 탐토상압고양(NH)처리시부개선APP/PS1쌍중전기인AD모형소서적공간학습화기억능력.방법 대APP/PS1쌍중전기인AD모형충서교배후산하적자대소서진행기인분형,대자대체10주시,취쌍중전기인소서20지,수궤분성A、B2조(매조10지).A조소서급여상압고양(40%O_2, 60%공기)처리,8h/d,지속8주;B조상규위양,작위대조.고양처리후진행Morris수미궁실험,분별검측각조소서재가시평태、은폐평태급공간탐색실험중조도평태적시간급수색적평균로정;행위학실험결속후,채용ELISA정량검측소서뇌내Aβ수평.결과 행위학실험결과:(1)가시평태하,2조소서조도평태적시간급수색적평균로정차이우현저성(P>0.05);(2)은폐평태하,고양처리조소서조도평태적시간급수색적평균로정교대조조명현축단(P<0.01);(3)공간탐색실험중,고양처리조소서경과평태적차수[(6.31±2.55)차]현저고정대조조[(3.13±1.59)7흠](P<0.01).ELISA결과현시,고양처리조소서대뇌피질급해마내Aβ40[(783.64±97.21)pg/ml화Aβ42(175.30±17.09)pg/ml]수평현저저우대조조[Aβ40(1251.59±42.29)pg/ml、Aβ42(286.83±12.96)pg/ml](P<0.01).결론 상압고양처리능현저개선AD모형소서공간학습기억장애;상압고양가능통과감소Aβ생성혹/화촉진혈관내피세포청제Aβ이발휘작용.
Objective To investigate whether normobaric hyperoxia exert neuroproteetive effect on APP/ PS1 double transgenic AD mouse model. Methods 20 APP/PS1 transgenic mice were randomly divided into 2 groups(A, B). Mice in group A were treated with 40% oxygen for 8 h per day, and lasted 8 weeks. Mice in group B were treated with normal air, as control. ELISA assay as well as behavioral test were used in the present study. Results Compared with normoxia-treated control, hyperoxia-treated mice had a significant lesser (P<0.01 ) to reach the platform in hidden platform test; furthermore, hyperoxia-treated mice (6.31 ± 2.55 ) had significantly much more platform-passing times in the probe trial (P < 0.01 ) than control (3.13 ±1.59), while mice in both groups had similar latency and pathlength to reach platform in visible platform (P > 0.05 ). EL1SA showed that Aβ40(783.64±97.21)pg/ml and Aβ42(175.30 ± 17.09) pg/ml were significantly decreased in hyperoxia-treated mice, compared with control[Aβ40 (1251.59 ± 42.29 ) pg/ml and Aβ42 (286.83 ± 12.96) pg/ml] (P< 0.01 ). Conclusion Treatment with hyperoxia significantly decreases Aβ deposition, and remarkably improves the capability of spatial learning and memory of APP/PS1 transgenic mice. Hyperoxia may exert its neuroprotective effect through decreasing Aβ generation or enhancing clearance of Aβ by endothelial cells.