nbqx對(duì)腦缺血再灌注后成年大鼠大腦少突膠質(zhì)前體細(xì)胞的保護(hù)作用

《nbqx對(duì)腦缺血再灌注后成年大鼠大腦少突膠質(zhì)前體細(xì)胞的保護(hù)作用》由會(huì)員上傳分享，免費(fèi)在線閱讀，更多相關(guān)內(nèi)容在學(xué)術(shù)論文-天天文庫。

1、NBQX對(duì)腦缺血再灌注后成年大鼠大腦少突膠質(zhì)前體細(xì)胞的保護(hù)作用作者：李華杰吳堅(jiān)盛世英朱林鳳張菊美【摘要】目的探討腦缺血再灌注后成年大鼠大腦少突膠質(zhì)前體細(xì)胞的變化及MK801和NBQX對(duì)其保護(hù)作用。方法以線栓法制作成年SD大鼠局灶性腦缺血再灌注模型(阻塞90min再灌注1d、7d和14d)，分別向其大腦皮質(zhì)缺血區(qū)立體定向注射5mmol/L的MK801和50mmol/L的NBQX各1μl，用免疫熒光組織化學(xué)法檢測(cè)腦缺血再灌注后成年大鼠早期大腦梗死中心區(qū)、梗死周邊區(qū)和缺血對(duì)側(cè)NG2和O4陽性細(xì)胞數(shù)量。結(jié)果腦缺血再

2、灌注后成年大鼠大腦皮質(zhì)梗死中心區(qū)NG2和O4陽性細(xì)胞逐漸減少，NBQX組大鼠NG2和O4陽性細(xì)胞數(shù)減少的幅度較少。腦缺血再灌注后梗死周邊區(qū)NG2和O4陽性細(xì)胞數(shù)逐漸增加，NBQX組大鼠增加更明顯，而MK801組與生理鹽水組無明顯差別。結(jié)論成年SD大鼠腦缺血再灌注后梗死周邊區(qū)少突膠質(zhì)前體細(xì)胞增多。NBQX對(duì)少突膠質(zhì)前體細(xì)胞早期的缺血性損傷有保護(hù)作用。【關(guān)鍵詞】缺血;再灌注;少突膠質(zhì)前體細(xì)胞;NBQX　　【Abstract】ObjectiveToexplorethechangeofoligodendrocytep

3、recursorcellsinadultratsafterfocalcerebralischemiaandtheprotectionofMK801andNBQXto9them.MethodsFocalcerebralischemiaandreperfusionmodelinmaleadultSDratswasestablishedbyoccludingtherightmiddlearterywith40nylonthread(bloodflowblockedfor90minutesandthenreperf

4、usionfor1day,7daysand14days.OnemicroliterMK801(5mmol/L)andNBQX(50mmol/L)wererespectivelyinjectedintothecerebralischemicareaofSDratsunderstereodirectionalinstrumentrightafterischemia.ThenNG2,O4positivecellsintheischemiccore,ischemicpenumbraandcontralateral

5、areaofratsweredeterminatedateachtimepointafterreperfusionbyimmunofluorescencehistochemistry.ResultsThenumberofNG2,O4positivecellswithintheischemiccoredecreasedsignificantlyateachtimepointwiththeNBQXgroupinlessamount.ThenumberofNG2andO4positivecellswithin

6、ischemicpenumbraincreasedgraduallyafterreperfusionwiththeNBQXgroupinhigheramount.ConclusionThemarkedincreaseofoligodendrocyteprecursorcellsisobservedintheperiinfarctareaduringthepostischemicreperfusionperiodintheadultratbrain.AndNBQXhassomeneuroprotectivee

7、ffecttooligodendrocyteprecursorcellsinpostischemicbraininjury.　　【Keywords】Ischemia;Reperfusion;Oligodendrocyte9precursorcells;NBQX　　興奮性氨基酸毒性損傷作用是腦創(chuàng)傷和腦卒中等中樞神經(jīng)系統(tǒng)(centralnervoussystem，CNS)疾病中神經(jīng)元死亡的主要因素之一[1]。而少突膠質(zhì)前體細(xì)胞(oligodendrocyteprecursorcells,OPC)膜上含有大量的興奮

8、性氨基酸受體[2]。MK801和NBQX分別是N甲基D天冬氨酸(NmethylDaspartate，NMDA)受體和α氨基3羥基5甲基4異唑丙酸鹽(alphaamino3hydroxy5methyl4isoxazolepropionate，AMPA)受體的拮抗劑。我們觀察了腦定向注射MK801和NBQX對(duì)大鼠腦缺血再灌注后早期大腦皮質(zhì)NG2和