【doc】 单侧颞叶皮质脑梗死大鼠空间认知能力与溶栓胶囊的干预效应

【doc】 单侧颞叶皮质脑梗死大鼠空间认知能力与溶栓胶囊的干预效应 单侧颞叶皮质脑梗死大鼠空间认知能力与 溶栓胶囊的干预效应 ISSN1671-5926CN21—1470/R删’rn中国临床康复2005年8月28日第9卷第32期 单侧颞叶皮质脑梗死大鼠空间认知能力与 溶栓胶囊的干预效应 董闽田,管兴志,匡培梓,高扬,管林初.匡培根,钱惠康(解放军 第一七五医院神经内科,福建省漳州市363o0O;解放军总医院神经 内科,北京市l00853;中国科学院0理研究所三室,北京市100101) 董闽田,男,1954年生,山东省滨州市人,汉族,1984年解放军第一军医大 学毕业,学士,主任医师,主要从事脑血管病,中枢系统感染. 摘要 背景:颞叶皮质人类和动物的学习记忆能J有关,它不仅接受听觉的 投射纤维,还j许多空间认知相关的脑区有密切关系 目的:观察单侧颞叶皮质腩梗死人鼠经溶栓胶囊治疗后空间认识能力 的改善情况. 设计:完全随机对照实验. 单位:解放军第L五医院神经内科,解放军总医院神经内科及中国科 学院心理研究所 材料:实验1998—08/1999—02在中同科学院心理研究所脑功能研究 室完成,选掸SD大鼠28只,随机分为3组:脑梗死组lO只,治疗组lO 只,假手术组8只 方法:立体定向光化学诱导制作脑梗死大鼠模水合氯醛麻醉,尾静 脉注射玫瑰红溶液20me/kg,左侧颞部切开皮,暴露颞骨,光导纤维 引导卤素灯冷光源,定向照射20min,面积2n’l[n一照射20rain后治疗 组腹腔注射溶栓胶囊生理盐水溶液(40g/1)200in~-/kg,脑梗死组腹腔 225 内注射等量生理盐水.假手术组尾静脉及腹腔注射生理盐水外,手术照 射条件相同. 主要观察指标:各组大鼠在Morris水迷宫中的训练成绩,包括:?反应 时.?搜索策略(分为边缘式记1分,随机式记2分,趋向式记3分,直 线式记4分). 结果:28只大鼠均进入结果分析.各组大鼠平均反应时比较:治疗 组和假手术组短于脑梗死组『第l天:58,5O,65s;第2天:24,27,46s; 第3天:14,l7,20s;第4天:l1,9,15s,(P<0.01)1,治疗组与假手术 组基本接近(P>0.05).?搜索策略评分:第l天可见假手术组及治 疗组稍高于脑梗死组,但不稳定(=1.167,P>0.05),第2天假手术 组高于脑梗死组【2.9,2.3分,(F=5.5,P<0.05)],但治疗组与脑梗死 组基本接近[2.6,2.3分,(F=3.34,P>0.05)],第3,4天治疗组均高于 脑梗死组[3.5,2.7分;3.7,3.3分,(F=8.92,14,P<0.O1)].治疗组与假 手术组基本接近(P>0.05). 结论:脑梗死早期给予溶栓胶囊治疗后,反应时明显缩短,搜索策略 逐渐由边缘式和随机式过渡到趋向式和直线式,说明溶栓胶囊可改 善脑缺血后的认知功能障碍,提高脑梗死大鼠的训练成绩. 主题词:脑梗塞/药物疗法;胶囊;颞叶;空间知觉;迷宫学习 中图分类号:R749.I文献标识码:A文章编号:167I一5926(2005)32—0223--03 董闽田管兴志匡培梓高扬管林初,匡培根钱惠康单侧颞叶皮质脑梗死大鼠空 间认知能力与溶栓胶囊的干预效应U1中国临床康复,2005,9(32):223—5 1wwwzglckfcoml (EditedbyZhangFJ/SunSG/SongLP/XiaoXL) ? BAsICREsEARCH? Expressionofprocaspase-3inthemousehippocampusafter transientforebrainischemia? LiuTian—hui,ChenRui laverCenter~BeijingFriendshipHospita1.AffiliateofCapitalUniversityof MedicalSciences.Beiiing100050China;DepartmentofBiochemistryand MolecularBiology,CapitalUniversityofMedicalSciences,Beijing loo054.China Correspondenceto:ProfessorChenRUi?.Master.Assistantinvestigator, DepartmentofBiochemistryandMolecularBiology,CapitalUniversityof Mediea1Sciences.Beiiing100054.Chinachenrui46@126.corll Received:2004—04—27Accepted:2005—0511f04/XN1 Abstract BACKGR0UND:Aftercerebralisehemia/reperfusioninjury.asaexecu— tionercaspase,proeaspase-3andeaspase-3-likeactivityincreasedsignifi— cantly.Weobserveboththedephosph()ry1aledandphosphorylatedprocas— pase-3,andtrytofindouttheirvariationsduringtheprocessesofcerebral ischemia/reperfusioninjury. 0BJECTIVE:()bservetheexpressionofprocaspase-3inhippocampusfol- lowingtransientforebrainischemia. DESIGN:Arandomizedandcontrolledexperiment. DEPARTMENT:DepartmentofBiochemistryandMolecularBiology. CapitalUniversityofMediea1Sciences. SETTING:1)epartmentofHyperbaricOxygenofBeijingChaoyangHospi— talAffiliatedtoCapitalUniversityofMedicalSciences METH0DS:Transientforebrainischemiawasreduce(1bvbilateralc0m. [noncarotidocclusionfBCCAO1fnr2Ominutes.Hippocampuswasob- tainedatreperfusiontimepointsof6hours.12hours.24hoursand48 hoursrespec-tivelyafter20minutesofBCCAO.Sham-operatedgroup didnotoccludebi-1ateralcommoncaroti(1.andhippocampuswasobtained atreperfusiontimepointof24hours.WesternBlottingwasusedtodetect the1evelofprocaspase.3. MAIN0UTC0MEMEASURES:Thecomparisonoftotalprocaspase.3. dephosphorylatedprocaspase-3andphosphorylatedproeaspase-3levelin hippocampusbetweeneachgroup RESULTS:Thirtymicewereinvolvedintheanalysis.?Totalproeaspase- 3level:Totalprocaspase-3levelincreasedinhippocampusatreperfusion timepointsof12hoursand24hourspost—BCCAOf9133.1?2216.3. 9355.9~1901.6,P<O.05).?Dephosphorylatedprocaspase一 3level:The dephosphorylatedprocaspase?-3levelincreasedinhippoeampusatreperfu?- siontimepointof24hourspost—BCCAO(7812.0~1625.1,3825.8~155.6,P <O.05).?Phosphorylatedprocaspase一 3level:Theincreasedexpression wasnotsignificantfP>O.051ascomparedwiththeexpressionlevelsin sham—operatedmice. CONCLUSION:Procaspase.3isupregulatedafterischemia/reperfusion. Theincrementofdephosphorylatedformofprocaspase-3washigherthan thatofphosphorylatedformofprocaspase-3uponcerebralischemia/reper- fusioninjury,whichindicatesthatcerebralischemiaZreperfusioninjurypos— siblyinducedthedephosphorylationofprocaspase?-3andpromoteditstrans?- formingintoactivatedfoln1. LiuTHChenRExpressionofprocaspase-3inthemousehippocampusaftertran- sientforebrainischemiaZhongguoLinchuangKartdCu2005;9(32}:225—7 (China} INTRoDUCTIoN Cerebralischemia/reperfusioninjurywillleadtoneuronalapopto— sis.Caspase一3isanestablishedproteaseknowntobeinvolvedin neuronalapoptosis.Lotsofevidencesimplicatedthatprocaspase一3 andcaspase?-3一likeactivityincreasedsignificantlyaftercerebralis.- chemia/reperfusioninjury.Procaspase一3hasbothdephosphory— latedandphosphorylatedform.Therewerealotofevidencesthat thedephosphorylatedformofprocaspase-3(32kDa)increasedafter cerebralischemia/reperfusion,butlittlewasknownaboutthe phosphorylatedformofprocaspase-3(35kDaorso).Inthepresent study,weexaminedbothdephosphorylatedandphosphorylated formofprocaspase一3afterischemia/reperfusion,andtriedtofind thepossiblemechanismofcerebralischemia/reperfusionandthe activationofprocaspase一3.