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ID:33073003
大小:10.82 MB
页数:45页
时间:2019-02-19
《疏血通对局灶性脑缺血大鼠神经细胞凋亡的影响》由会员上传分享,免费在线阅读,更多相关内容在学术论文-天天文库。
1、河北医科大学硕士学位论文疏血通对局灶性脑缺血大鼠神经细胞凋亡的影响姓名:卢军栋申请学位级别:硕士专业:神经病学指导教师:王晓鹏201203中文摘要疏血通对局灶性脑缺血大鼠神经细胞凋亡的影响摘要目的:通过观察中药疏血通(shuxuetongSXT)对缺血性脑卒中大鼠一氧化氮(niticoxideNO)、神经原型一氧化氮合酶(neuronalnitricoxidesynthasenNOS)及bcl.2、bax蛋白表达的影响,来探讨SXT抑制神经细胞凋亡,保护缺血性脑损伤的可能作用机制,为SXT治疗缺血性脑卒中在临床上的应用提供更深层次的理论依据。方法:选
2、用健康SD大鼠78只雌雄各半,随机分为:假手术组、缺血对照组和SXT不同剂量组、尼莫地平阳性对照组,SXT又分为3个剂量组:低0.3ml/kg/d、中0.6ml/kg/d、高1.2ml/kg/d。分别给予大鼠不同剂量的SXT进行预处理,以线栓法阻塞大鼠右侧大脑中动脉制备局灶性脑缺血模型(middlecerebralarteryocclusionMCAO),12h后行神经功能缺失评分,断头取脑制备脑组织匀浆测NO含量、免疫组化SABC法染色对nNOS及凋亡相关基因bcl.2、bax蛋白进行定量分析,统计大鼠缺血侧大脑皮层顶叶缺血半暗带区每高倍镜视野nN
3、OS及bcl-2蛋白、bax蛋白的阳性表达率[阳性细胞数/(阳性细胞数+阴性细胞数)×100%】。结果:。1.SXT组脑组织匀浆中NO含量较单纯缺血对照组减少Q4、ax蛋白表达,从而抑制细胞凋亡来减少脑缺血后迟发性神经元损伤,挽救缺血半暗区神经细胞,减轻脑损害,保护脑组织。关词键:SXT;缺血性脑卒中;nNOS;细胞凋亡英文摘要TheApoptosisinhibitionandneuroprotectiveeffectsofSXTon1^o·’·-■●■‘ocalCerebraltschemlalnratsABSTRACTObjective:Tostudythefunctionofapoptosisinhibitionandneuroprotectiveeffectsinfocalcerebralischemi5、amjurybyanalyzingthechangeofNO,nNOS,bcl·2andbaxproteininratsaftertreatmentwithSXT,andpotentiallyprovideinformationtothepreventionandtreatmentincerebralarterialthrombosis.Methods:ThehealthySDratsseventyeightwererandomlydividedintothesham—operativegroup,focalcerebralischemiagroup6、,SXTgroupandNimodipinegroup.111eSXTgroupwasdividedinto3groupsaccordingtodifferentdose:0.3ml/kg/d,0.6ml/kg/dand1.2ml/kg/d,respectively.ThentheratswerepretreatedwithSXTindifferentdosebeforeestablishingmiddlecerebralarteryocclusion(MCAO)model.After12hfocalcerebralischemia,theneuro7、logicalfunctionwasestimatedandthecontentofnitrogenniticoxide(NO)inbraintissuewasmeasured.Meanwhile,thegeneexpressionsofbcl·2,baxandnNOSwerestudiedbySABCstaining.Thepositivecellrateofbcl一2andbaxproteinincerebralcortexwereobservedbytheimmunohistochemicalmethodandimageanalysis.Res8、ults:1.ThecontentofNOwasdecreasedinSXTgroup.2.Especial
4、ax蛋白表达,从而抑制细胞凋亡来减少脑缺血后迟发性神经元损伤,挽救缺血半暗区神经细胞,减轻脑损害,保护脑组织。关词键:SXT;缺血性脑卒中;nNOS;细胞凋亡英文摘要TheApoptosisinhibitionandneuroprotectiveeffectsofSXTon1^o·’·-■●■‘ocalCerebraltschemlalnratsABSTRACTObjective:Tostudythefunctionofapoptosisinhibitionandneuroprotectiveeffectsinfocalcerebralischemi
5、amjurybyanalyzingthechangeofNO,nNOS,bcl·2andbaxproteininratsaftertreatmentwithSXT,andpotentiallyprovideinformationtothepreventionandtreatmentincerebralarterialthrombosis.Methods:ThehealthySDratsseventyeightwererandomlydividedintothesham—operativegroup,focalcerebralischemiagroup
6、,SXTgroupandNimodipinegroup.111eSXTgroupwasdividedinto3groupsaccordingtodifferentdose:0.3ml/kg/d,0.6ml/kg/dand1.2ml/kg/d,respectively.ThentheratswerepretreatedwithSXTindifferentdosebeforeestablishingmiddlecerebralarteryocclusion(MCAO)model.After12hfocalcerebralischemia,theneuro
7、logicalfunctionwasestimatedandthecontentofnitrogenniticoxide(NO)inbraintissuewasmeasured.Meanwhile,thegeneexpressionsofbcl·2,baxandnNOSwerestudiedbySABCstaining.Thepositivecellrateofbcl一2andbaxproteinincerebralcortexwereobservedbytheimmunohistochemicalmethodandimageanalysis.Res
8、ults:1.ThecontentofNOwasdecreasedinSXTgroup.2.Especial
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