中华创伤杂志
中華創傷雜誌
중화창상잡지
Chinese Journal of Traumatology
2012年
2期
175-178
,共4页
夏学巍%董宇为%杜贻庆%阳永东%李普阳%孙帅奇
夏學巍%董宇為%杜貽慶%暘永東%李普暘%孫帥奇
하학외%동우위%두이경%양영동%리보양%손수기
脑损伤%海马%认知障碍
腦損傷%海馬%認知障礙
뇌손상%해마%인지장애
Brain injuries%Hippocampus%Cognitive impairment
目的 观察创伤性脑损伤(traumatic brain injury,TBI)大鼠在Morris水迷宫中学习、记忆能力与大鼠海马区突触后致密物蛋白质95(postsynaptic density 95,PSD - 95)表达变化的关系. 方法 采用完全随机设计将SD大鼠分为TBI组和对照组.TBI组采用冲击加速度脑损伤方式建立模型,通过Morris水迷宫试验观察TBI组和对照组脑损伤后1周的学习、记忆能力,采用免疫蛋白电泳技术观察大鼠海马区脑损伤后1,3,7 d PSD- 95的表达. 结果 与对照组比较,TBI组伤后1周水迷宫逃避潜伏期延长,并且表现较脑损伤后前3d延长明显;蛋白电泳条带灰度半定量分析结果显示PSD - 95在受伤后1周逐渐减少(P<0.01). 结论 TBI可致大鼠海马区PSD - 95表达减少,这可能是导致学习、记忆障碍的机制之一.
目的 觀察創傷性腦損傷(traumatic brain injury,TBI)大鼠在Morris水迷宮中學習、記憶能力與大鼠海馬區突觸後緻密物蛋白質95(postsynaptic density 95,PSD - 95)錶達變化的關繫. 方法 採用完全隨機設計將SD大鼠分為TBI組和對照組.TBI組採用遲擊加速度腦損傷方式建立模型,通過Morris水迷宮試驗觀察TBI組和對照組腦損傷後1週的學習、記憶能力,採用免疫蛋白電泳技術觀察大鼠海馬區腦損傷後1,3,7 d PSD- 95的錶達. 結果 與對照組比較,TBI組傷後1週水迷宮逃避潛伏期延長,併且錶現較腦損傷後前3d延長明顯;蛋白電泳條帶灰度半定量分析結果顯示PSD - 95在受傷後1週逐漸減少(P<0.01). 結論 TBI可緻大鼠海馬區PSD - 95錶達減少,這可能是導緻學習、記憶障礙的機製之一.
목적 관찰창상성뇌손상(traumatic brain injury,TBI)대서재Morris수미궁중학습、기억능력여대서해마구돌촉후치밀물단백질95(postsynaptic density 95,PSD - 95)표체변화적관계. 방법 채용완전수궤설계장SD대서분위TBI조화대조조.TBI조채용충격가속도뇌손상방식건립모형,통과Morris수미궁시험관찰TBI조화대조조뇌손상후1주적학습、기억능력,채용면역단백전영기술관찰대서해마구뇌손상후1,3,7 d PSD- 95적표체. 결과 여대조조비교,TBI조상후1주수미궁도피잠복기연장,병차표현교뇌손상후전3d연장명현;단백전영조대회도반정량분석결과현시PSD - 95재수상후1주축점감소(P<0.01). 결론 TBI가치대서해마구PSD - 95표체감소,저가능시도치학습、기억장애적궤제지일.
Objective To investigate the relation of learning and memory with the expression of postsynaptic density 95 (PSD-95) in traumatic brain injury (TBI) rats in Morris water maze. Methods Forty adult male Sprague-Dawley rats were randomly assigned to the TBI group and control group.The TBI group was produced using the impact acceleration injury model.Morris water maze memory paradigm was used to assess the learning and memory function in both groups one week after injury.Protein electro-phoresis was used to observe the expression of PSD-95 1,3,7 d after TBI. Results Compared with the control group,the TBI group showed a longer latency in the Morris water maze after one week,significantly longer than the latency in the first three days after TBI.The quantification of PSD-95 in the hippocampus was gradually reduced at one week after TBI ( P < 0.01 ). Conclusion TBI may decrease expression of PSD-95 in the hippocampus of the rats,as may be one of the mechanisms for impairments of learning and memory of rats.