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ID:33016576
大小:3.77 MB
页数:41页
时间:2019-02-19
《硒蛋白s在缺血性脑卒中大鼠脑组织的表达》由会员上传分享,免费在线阅读,更多相关内容在行业资料-天天文库。
1、m糸大学俩■学位诧文组织,梗塞中心处、缺血半暗带)进行western—blot实验。整个过程运用神经功能缺损评分、梗塞后脑组织体积变化、TTC染色和lie染色确定线栓法制作脑梗塞模型的成功性和井确定梗塞部位,运用尼氏染色、免疫缎化和westernblot检测缺血后脑组织神经元损伤情况、星形胶质细胞活动情况及sols在不同部位、时问点表达变化及参与脑梗塞发生的可能机制。进行数据整理分析.得出SelS表达情况。结果:I_行为学观察:大鼠脑缺血再灌注后神经功能缺损症状较假手术组明显(p2、j%手术大鼠于缺血再灌注后24h神经功能缺损症状遮高峰,根据ZeaLonga评分,缺血再灌注后3h神经功能缺损评分达2-3分者方可用于实验。2脑组织缺血损伤:TTC染色示线栓法阻塞大脑中动脉的脑缺血损伤主要引起同倒半球大脑中动脉供应的运动感觉皮质区和纹状体区组织梗死,将该侧脑组织分为梗塞中心区和梗塞周围区;缺血再灌注后24h的脑组织梗塞侧表面积增大,而3d和7d的脑组织梗塞侧表面积减少.7d时更明显:梗塞中心可见细胞肿胀、萎缩,周边残留空穴.缺血半暗带区则正常细胞和缺血损伤细胞并存:梗死中心可见神经元在缺血再灌注后12h数量明显减少,星形腔质细3、胞在3d时开始出现明显减少(p4、.脑梗搴部位固定可靠,梗塞中心区神经细胞逐渐坏死消失.缺血半暗带出现胶质细胞增q:。2.Se】s在缺m性晌卒中的腑组织缺血半暗带区表达匿增高。3.SeIs在缺m中心和缺血半昭带的表达与(;FAP的表达模式一致,Sels抗炎作用关键词:脑缺血:硒蛋白s:炎症:星形胶质细胞盘一,。.:。一:≯蛰戮再譬一F躞嚣;髑蔫‘。;f.一1≤,川菖一1.】叩t—L_._,,J,■<一寤;气1U.一_r1hI_一麓SelenoproteinSExpressionintheRatBrainfollowingFocalCerebraIIschemiaMajor:Ne5、urologyPostgraduate:LiuLixiaFulors:ZhouShengnianABSTRACTobjettives:Strokehasbeenthethirdleadingcaoseofdeathafterheartdiseasesandcancer,andalsothemostcommoncauseofcomplexdisabilityinadultsaroundtheworldRecentstudiesoncerebralischemicstrokehavedemonstratedtheimportanceoftheinf6、lammatoryresponseOngoinginflammatoryinsultshavebeenimplicatedasasecondarymechanismunderlyingneuronalinjury—inducedbyischemia,andanti-inflammatorystrategieshavegainedconsiderableinterestS(SelS).whichisanendoplasmicreticulum(ER)residentprotein.isknowntopromotecellsurvivalbyreg7、ulatinginflammationMoreover.SelShasbeenshowntoberesponsivetoischemiainculturedastroc”esAFinnishreportrevealedthatavariationintheSelSgenelocusisassociatedwithahigherpredispositiontoischemicstrokeinhumans,suggestingacrucialroleforSelSinprotectionagainstbrainischemiaHowever.the8、time-courseofSelSexpressionfollowingcerebralischemiainvivoremainsunclearInt
2、j%手术大鼠于缺血再灌注后24h神经功能缺损症状遮高峰,根据ZeaLonga评分,缺血再灌注后3h神经功能缺损评分达2-3分者方可用于实验。2脑组织缺血损伤:TTC染色示线栓法阻塞大脑中动脉的脑缺血损伤主要引起同倒半球大脑中动脉供应的运动感觉皮质区和纹状体区组织梗死,将该侧脑组织分为梗塞中心区和梗塞周围区;缺血再灌注后24h的脑组织梗塞侧表面积增大,而3d和7d的脑组织梗塞侧表面积减少.7d时更明显:梗塞中心可见细胞肿胀、萎缩,周边残留空穴.缺血半暗带区则正常细胞和缺血损伤细胞并存:梗死中心可见神经元在缺血再灌注后12h数量明显减少,星形腔质细
3、胞在3d时开始出现明显减少(p4、.脑梗搴部位固定可靠,梗塞中心区神经细胞逐渐坏死消失.缺血半暗带出现胶质细胞增q:。2.Se】s在缺m性晌卒中的腑组织缺血半暗带区表达匿增高。3.SeIs在缺m中心和缺血半昭带的表达与(;FAP的表达模式一致,Sels抗炎作用关键词:脑缺血:硒蛋白s:炎症:星形胶质细胞盘一,。.:。一:≯蛰戮再譬一F躞嚣;髑蔫‘。;f.一1≤,川菖一1.】叩t—L_._,,J,■<一寤;气1U.一_r1hI_一麓SelenoproteinSExpressionintheRatBrainfollowingFocalCerebraIIschemiaMajor:Ne5、urologyPostgraduate:LiuLixiaFulors:ZhouShengnianABSTRACTobjettives:Strokehasbeenthethirdleadingcaoseofdeathafterheartdiseasesandcancer,andalsothemostcommoncauseofcomplexdisabilityinadultsaroundtheworldRecentstudiesoncerebralischemicstrokehavedemonstratedtheimportanceoftheinf6、lammatoryresponseOngoinginflammatoryinsultshavebeenimplicatedasasecondarymechanismunderlyingneuronalinjury—inducedbyischemia,andanti-inflammatorystrategieshavegainedconsiderableinterestS(SelS).whichisanendoplasmicreticulum(ER)residentprotein.isknowntopromotecellsurvivalbyreg7、ulatinginflammationMoreover.SelShasbeenshowntoberesponsivetoischemiainculturedastroc”esAFinnishreportrevealedthatavariationintheSelSgenelocusisassociatedwithahigherpredispositiontoischemicstrokeinhumans,suggestingacrucialroleforSelSinprotectionagainstbrainischemiaHowever.the8、time-courseofSelSexpressionfollowingcerebralischemiainvivoremainsunclearInt
4、.脑梗搴部位固定可靠,梗塞中心区神经细胞逐渐坏死消失.缺血半暗带出现胶质细胞增q:。2.Se】s在缺m性晌卒中的腑组织缺血半暗带区表达匿增高。3.SeIs在缺m中心和缺血半昭带的表达与(;FAP的表达模式一致,Sels抗炎作用关键词:脑缺血:硒蛋白s:炎症:星形胶质细胞盘一,。.:。一:≯蛰戮再譬一F躞嚣;髑蔫‘。;f.一1≤,川菖一1.】叩t—L_._,,J,■<一寤;气1U.一_r1hI_一麓SelenoproteinSExpressionintheRatBrainfollowingFocalCerebraIIschemiaMajor:Ne
5、urologyPostgraduate:LiuLixiaFulors:ZhouShengnianABSTRACTobjettives:Strokehasbeenthethirdleadingcaoseofdeathafterheartdiseasesandcancer,andalsothemostcommoncauseofcomplexdisabilityinadultsaroundtheworldRecentstudiesoncerebralischemicstrokehavedemonstratedtheimportanceoftheinf
6、lammatoryresponseOngoinginflammatoryinsultshavebeenimplicatedasasecondarymechanismunderlyingneuronalinjury—inducedbyischemia,andanti-inflammatorystrategieshavegainedconsiderableinterestS(SelS).whichisanendoplasmicreticulum(ER)residentprotein.isknowntopromotecellsurvivalbyreg
7、ulatinginflammationMoreover.SelShasbeenshowntoberesponsivetoischemiainculturedastroc”esAFinnishreportrevealedthatavariationintheSelSgenelocusisassociatedwithahigherpredispositiontoischemicstrokeinhumans,suggestingacrucialroleforSelSinprotectionagainstbrainischemiaHowever.the
8、time-courseofSelSexpressionfollowingcerebralischemiainvivoremainsunclearInt
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