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ID:33959253
大小:2.06 MB
页数:54页
时间:2019-03-02
《sphk2在急性脑梗死大鼠脑组织的动态表达与氧化苦参碱的神经保护作用》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、中文摘要处死,用干湿重法测定脑组织含水量,用2%2,3,5.三苯基四唑氮红(triphenyltetrazoliumchloride,Trc)染色法测算脑梗死体积,用免疫组化、WesternBlot及RT-PCR来观察SphK2及claudin.5的表达情况。结果:1与正常对照组相比,MCAO组SphK2于脑缺血后12h开始升高,72h达高峰俨<0.05)。2OMT可以改善神经功能的缺失,降低脑水肿以及脑梗死面积。与MCAO组相比,OMT组行为学评分下降(尸<0.05);脑水肿含量减少(MCAOVS.OMT:83
2、.08±0.56VS.81.00±0.43,P<0.01);脑梗死面积减少(MCAOVS.OMT:46.66±3.36VS.26.01±6.10,P3、脑屏障的通透性。与假手术组相比,脑缺血后claudin.5表达明显下降。RT-PCR以及WesternBlot均显示OMT可以上调缺血脑组织内claudin-5的表达(RT-PCR:MCAOVS.OMT:0.47±0.04VS.O.55±0.01,P<0.05;WesternBlot:MCAOVS.OMT:O.95±0.04VS.1.25±O.14,P<0.05)。结论:SphK2在脑缺血的损伤过程中表达上调,给予OMT干预后可以有效减少神经系统损伤以及组织损伤。其作用可能与下调SphK2,抑制凋亡;上调clau4、din.5,改善血脑屏障有关。用关键词:氧化苦参碱;脑缺血;鞘氨醇激酶;血脑屏障;神经保护作2英文摘要ThelongitudinalexpressionofSphK2inacutecerebralischemiainratsandtheneuroprotectiveeffectofoxymatdneABSTRACTObjective:Ischemiawi廿1highmortalityandseriousdisabilityisthemostconllnontypeofcerebralvasculardisease5、.Thepathologicalmechanismforischemicinjurywasaperplexingcascadereaction,theperturbationofcalciumhomeostasisplaysanimportantroleincerebralischemicpathogenesis.TheintracellularcalciumoverloadactivatedkindsofenzymesregulatedbyCa,:inducedmembranephospholipidresol6、vedandbrokedowncytoskeletonwithsubsequentcelldeath.Sphingosinekinase(SphK)isacriticalenzymethatcatalyzesthephosphorylationofsphingosinetosphingosine一1一phosphate.Thecatalyticactivityandspecificsubcellularlocalizationalsocontributestothepro—apoptoticeffectofSph7、K2,whichaffecttheintracellularC扩.Oxymatrine(OMT)isanalkaloidextractedfromSophoraflavescensAiranditsmolecularformulaisC15H24N202,wi廿latetracyclicquinolizinestructure.Inbothpreclinicalandclinicalstudies,ithasbeenconfirmedtopossessavarietyofbiologicalactivitiesi8、ncludinganti—inflammatory,anti-oxidant,anti—cancerandanti—anaphylaxisproperties.Inrecentyears,therearemanystudiesconductedonOMT,mostofthemarefocusedonanti-hepatitisandanti—carcinoma,butth
3、脑屏障的通透性。与假手术组相比,脑缺血后claudin.5表达明显下降。RT-PCR以及WesternBlot均显示OMT可以上调缺血脑组织内claudin-5的表达(RT-PCR:MCAOVS.OMT:0.47±0.04VS.O.55±0.01,P<0.05;WesternBlot:MCAOVS.OMT:O.95±0.04VS.1.25±O.14,P<0.05)。结论:SphK2在脑缺血的损伤过程中表达上调,给予OMT干预后可以有效减少神经系统损伤以及组织损伤。其作用可能与下调SphK2,抑制凋亡;上调clau
4、din.5,改善血脑屏障有关。用关键词:氧化苦参碱;脑缺血;鞘氨醇激酶;血脑屏障;神经保护作2英文摘要ThelongitudinalexpressionofSphK2inacutecerebralischemiainratsandtheneuroprotectiveeffectofoxymatdneABSTRACTObjective:Ischemiawi廿1highmortalityandseriousdisabilityisthemostconllnontypeofcerebralvasculardisease
5、.Thepathologicalmechanismforischemicinjurywasaperplexingcascadereaction,theperturbationofcalciumhomeostasisplaysanimportantroleincerebralischemicpathogenesis.TheintracellularcalciumoverloadactivatedkindsofenzymesregulatedbyCa,:inducedmembranephospholipidresol
6、vedandbrokedowncytoskeletonwithsubsequentcelldeath.Sphingosinekinase(SphK)isacriticalenzymethatcatalyzesthephosphorylationofsphingosinetosphingosine一1一phosphate.Thecatalyticactivityandspecificsubcellularlocalizationalsocontributestothepro—apoptoticeffectofSph
7、K2,whichaffecttheintracellularC扩.Oxymatrine(OMT)isanalkaloidextractedfromSophoraflavescensAiranditsmolecularformulaisC15H24N202,wi廿latetracyclicquinolizinestructure.Inbothpreclinicalandclinicalstudies,ithasbeenconfirmedtopossessavarietyofbiologicalactivitiesi
8、ncludinganti—inflammatory,anti-oxidant,anti—cancerandanti—anaphylaxisproperties.Inrecentyears,therearemanystudiesconductedonOMT,mostofthemarefocusedonanti-hepatitisandanti—carcinoma,butth
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