中国老年学杂志
中國老年學雜誌
중국노년학잡지
CHINESE JOURNAL OF GERONTOLOGY
2010年
4期
495-498
,共4页
张晓裕%何利明%侯军代%肖飞%罗焕敏
張曉裕%何利明%侯軍代%肖飛%囉煥敏
장효유%하리명%후군대%초비%라환민
去痴灵%阿尔茨海默病%学习记忆%突触%突触体素
去癡靈%阿爾茨海默病%學習記憶%突觸%突觸體素
거치령%아이자해묵병%학습기억%돌촉%돌촉체소
Quchiling%Alzheimer's disease%Learning and memory%Synapse%Synaptophysin
目的 观察去痴灵对阿尔茨海默病(AD)小鼠学习记忆以及脑内突触体素(synaptophysin,SYN)表达的影响.方法 选用昆明种小鼠,右侧脑室注射β-淀粉样蛋白25-35(Aβ25-35)制备AD动物模型.造模1 w后,治疗组分别灌胃低、中、高剂量(3.05、6.10、12.20 g·kg~(-1)·d~(-1))去痴灵,以石杉碱甲为阳性对照药,连续28 d.给药结束后,对各组小鼠进行Morris水迷宫测试、脑组织SYN含量测定以及海马CA1区病理结构观察.结果 与模型组比较,去痴灵各剂量组均明显缩短水迷宫逃避潜伏期(P<0.05),中、高剂量组跨越平台次数显著增加(P<0.05);各治疗组AchE阳性纤维密度明显增加(P<0.05),脑内SYN含量明显升高(P<0.05),突触结构改善明显;各治疗组上述指标组间比较差异不显著(P>0.05).结论 去痴灵可明显改善Aβ所致的小鼠记忆障碍及突触丧失,其脑内突触再生,突触体素含量增加可能是去痴灵改善AD记忆的重要途径之一.
目的 觀察去癡靈對阿爾茨海默病(AD)小鼠學習記憶以及腦內突觸體素(synaptophysin,SYN)錶達的影響.方法 選用昆明種小鼠,右側腦室註射β-澱粉樣蛋白25-35(Aβ25-35)製備AD動物模型.造模1 w後,治療組分彆灌胃低、中、高劑量(3.05、6.10、12.20 g·kg~(-1)·d~(-1))去癡靈,以石杉堿甲為暘性對照藥,連續28 d.給藥結束後,對各組小鼠進行Morris水迷宮測試、腦組織SYN含量測定以及海馬CA1區病理結構觀察.結果 與模型組比較,去癡靈各劑量組均明顯縮短水迷宮逃避潛伏期(P<0.05),中、高劑量組跨越平檯次數顯著增加(P<0.05);各治療組AchE暘性纖維密度明顯增加(P<0.05),腦內SYN含量明顯升高(P<0.05),突觸結構改善明顯;各治療組上述指標組間比較差異不顯著(P>0.05).結論 去癡靈可明顯改善Aβ所緻的小鼠記憶障礙及突觸喪失,其腦內突觸再生,突觸體素含量增加可能是去癡靈改善AD記憶的重要途徑之一.
목적 관찰거치령대아이자해묵병(AD)소서학습기억이급뇌내돌촉체소(synaptophysin,SYN)표체적영향.방법 선용곤명충소서,우측뇌실주사β-정분양단백25-35(Aβ25-35)제비AD동물모형.조모1 w후,치료조분별관위저、중、고제량(3.05、6.10、12.20 g·kg~(-1)·d~(-1))거치령,이석삼감갑위양성대조약,련속28 d.급약결속후,대각조소서진행Morris수미궁측시、뇌조직SYN함량측정이급해마CA1구병리결구관찰.결과 여모형조비교,거치령각제량조균명현축단수미궁도피잠복기(P<0.05),중、고제량조과월평태차수현저증가(P<0.05);각치료조AchE양성섬유밀도명현증가(P<0.05),뇌내SYN함량명현승고(P<0.05),돌촉결구개선명현;각치료조상술지표조간비교차이불현저(P>0.05).결론 거치령가명현개선Aβ소치적소서기억장애급돌촉상실,기뇌내돌촉재생,돌촉체소함량증가가능시거치령개선AD기억적중요도경지일.
Objective To investigate the effects of Quchiling on the learning and memory and synaptophysin(SYN) expression of brain in Alzheimer's disease (AD) model mice.Methods AD mice model was established by β-amyloid peptide 25-35 injection into right lateral ventricle.One week later,the therapeutic groups were given Quchiling through gastric gavage for 28 days.Huperzine A was used as a positive control drug.Subsequently,the test of Morris water-maze,the expression of SYN,the dense of AchE!positive fibrils and the observation of ultrastructure of synapses in brain were applied to evaluate the effects of Quchiling on the AD model mice.Results Compared with AD model group,the mice administered by different doses of Quchiling had shorter escape latency and more platform-crossing times except the group treated with low dose Quchiling (P<0.05).Furthermore,Quchiling increased the dense of AchE positive fibrils and upregulated the expression of SYN (P<0.05).There was no remarkably difference between all the therapeutic groups (P>0.05).Conclusions Quchiling increases the content of the cerebric SYN,and restores the impaired synapse structure,which maybe contributed to the improvement of learning and memory in the mice with AD.