欢迎来到天天文库
浏览记录
ID:5317644
大小:951.14 KB
页数:5页
时间:2017-12-08
《trek-1通道活性改变对大鼠局灶性脑缺血后细胞凋亡和凋亡相关蛋白的影响》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、神经损伤与功能重建·2014年1月·第9卷·第1期11·论著·TREK一1通道活性改变对大鼠局灶性脑缺血后细胞凋亡和凋亡相关蛋白的影响刘阳,孙谦,王伟,谢敏杰摘要目的:观察双孔钾通道TREK1活性改变对大鼠局灶性脑缺血后细胞凋亡和凋亡相关蛋白的影响。作者单位方法:45只大鼠随机分为假手术组(10只)、对照组(1O只)和干预组(25只)。建立大鼠光化学脑缺血模型,华中科技大学同济医假手术组不注射玫瑰红,干预组侧脑室注射不同浓度(100p,mol/L、250i~mol/L、500Ixmol/L、1mmol/L)亚麻学院附属同济医院神酸(LIN),对照组注射等量生理盐水。应
2、用免疫荧光双标法观察正常生理情况下TREK.1在大脑神经细胞经内科中的表达,TUNEL及DAPI双标法检测缺血边缘区细胞凋亡,Westernblot法检测B细胞淋巴瘤.2武汉430030(Bc1.2)、Bc1.2相关x蛋白(Bax)、磷酸化细胞外信号调节激酶(p-erk)表达。结果:正常生理情况下,基金项目TREK.1在神经元和星形胶质细胞中均有表达。与假手术组相比,对照组大量细胞凋亡,Bc1.2/Bax值下降,国家自然科学基金p-erk蛋白增加(P<0.05);与对照组比较,干预组细胞凋亡显著减少,Bc1.2/Bax值上升,p-erk蛋白降低(No.30971007
3、);(P4、ollowingFocalCerebralIschemiaUUYang,SUNQian.WANGWei,XIEMin-jie.通讯作者DepartmentofNeurology,TongfiHospital,TongfiMedicalCollege,HuazhongUniversityofScienceandcJ1-谓j敏杰nology,Wuhan430030,Chh2aAbstractObjective:ToinvestigatetheeffectofTREK一1channelactivityoncellapoptosisandtheproteinex-xiemj25、000@yahoo.pressionofBcl一2andBaxafterfocalcerebralischemiainrats.Methods:Forty-fiveratswererandomlyassignedC0m.Cnintosham—operated(n=10),vehicle—treatment(n=l0),andinterventiongroups(n=_25).Photochemicalischemiawasperformedandsham—operatedanimalsweregivensalineinsteadofRoseBenga1.Alpha—l6、ineonicacidwasadministratedi.c.v(100p~mol/L,250~mol/L,500txmol/L,or1rnmol/L).Vehicletreatedanimalsreceivedthesamevolumesof0.9%NaC1.ThecellulardistributionofTREK一1inratbrainwasdetectedbyimmunohistochem—icalstaining.DoublestainingofTUNELandDAP1wasperformedtodeterminethepercentageofcelldea7、thandtheproteinexpressionofB—celllymphoma一2(Bcl-2),Bcl一2一associatedXprotein(Bax)andPhosphorylatedExtra—cellularSignal—RegulatedKinase(p—erk)wasdetectedbywesternblot.Results:TREK-limmunoreactivetywasexpressedintheGFAPpositiveastrocytesandNeuNpositiveneuronsinthecerebralcodex.Com
4、ollowingFocalCerebralIschemiaUUYang,SUNQian.WANGWei,XIEMin-jie.通讯作者DepartmentofNeurology,TongfiHospital,TongfiMedicalCollege,HuazhongUniversityofScienceandcJ1-谓j敏杰nology,Wuhan430030,Chh2aAbstractObjective:ToinvestigatetheeffectofTREK一1channelactivityoncellapoptosisandtheproteinex-xiemj2
5、000@yahoo.pressionofBcl一2andBaxafterfocalcerebralischemiainrats.Methods:Forty-fiveratswererandomlyassignedC0m.Cnintosham—operated(n=10),vehicle—treatment(n=l0),andinterventiongroups(n=_25).Photochemicalischemiawasperformedandsham—operatedanimalsweregivensalineinsteadofRoseBenga1.Alpha—l
6、ineonicacidwasadministratedi.c.v(100p~mol/L,250~mol/L,500txmol/L,or1rnmol/L).Vehicletreatedanimalsreceivedthesamevolumesof0.9%NaC1.ThecellulardistributionofTREK一1inratbrainwasdetectedbyimmunohistochem—icalstaining.DoublestainingofTUNELandDAP1wasperformedtodeterminethepercentageofcelldea
7、thandtheproteinexpressionofB—celllymphoma一2(Bcl-2),Bcl一2一associatedXprotein(Bax)andPhosphorylatedExtra—cellularSignal—RegulatedKinase(p—erk)wasdetectedbywesternblot.Results:TREK-limmunoreactivetywasexpressedintheGFAPpositiveastrocytesandNeuNpositiveneuronsinthecerebralcodex.Com
此文档下载收益归作者所有