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1、新生大鼠缺氧缺血腦損傷時腦組織STAT3信號通路的作用鄧睿1周立剛1趙鳳艷2張莉2李德淵2母得志2（400013重慶，重慶市婦幼保健院新生兒科；610041四川成都，四川大學(xué)華西第二醫(yī)院兒科2）[摘要]目的研究信號轉(zhuǎn)導(dǎo)和轉(zhuǎn)錄激活因子3（STAT3）信號通路在新生大鼠缺氧缺血（HI）腦損傷中的作用。方法采用Rice法建立7日齡SD大鼠缺氧缺血腦損傷（HIBD）模型，同時設(shè)立對照。于HI后4h、6h、8h、12h和24h取腦，采用免疫組織化學(xué)法及Westernblot檢測STAT3、磷酸化STAT3（p-STAT3）及血管內(nèi)
2、皮生長因子（VEGF）的表達(dá)與分布，TUNEL法檢測神經(jīng)細(xì)胞凋亡。結(jié)果HI組p-STAT3蛋白表達(dá)在HI后4h升高，6h達(dá)高峰，8~12h逐漸下降，均明顯高于假手術(shù)組，差異有統(tǒng)計(jì)學(xué)意義（P﹤0.05）。而STAT3總蛋白表達(dá)與假手術(shù)組比較，差異無統(tǒng)計(jì)學(xué)意義（P﹥0.05）。VEGF于HI后各時間點(diǎn)均明顯高于假手術(shù)組，差異有統(tǒng)計(jì)學(xué)意義（P﹤0.05）。TUNEL染色陽性細(xì)胞數(shù)于HI后24h達(dá)高峰，明顯高于假手術(shù)組，差異有統(tǒng)計(jì)學(xué)意義(P﹤0.01)。結(jié)論新生大鼠HI后，p-STAT3蛋白表達(dá)增高，可能誘導(dǎo)VEGF表達(dá)，對神經(jīng)
3、元的凋亡具有抑制作用。[關(guān)鍵詞]信號轉(zhuǎn)導(dǎo)和轉(zhuǎn)錄激活因子；STAT3；血管內(nèi)皮生長因子；凋亡；缺氧缺血性腦損傷；新生大鼠[中圖分類號]R-72[文獻(xiàn)標(biāo)識碼]A[文章編號]ThefunctionofSTAT3signalingpathwayinneonatalratsfollowinghypoxic-ischemiabraindamageAbstract：ObjectiveToinvestigatethefunctionofSTAT3signalingpathwayinneonatalratsunderhypoxiaisch
4、emia(HI)condition.MethodsHypoxic-ischemiabraininjuryanimalmodelwasmadeusing7-day-oldSDratsaccordingtoRice-Vannuccimodel,andcomparativestudiesweremadewithashamgroup.Braintissueswerecollectedafter4h、6h、8h、12hand24hofrecoveryfromHI.Immunohistochemistryandwesternblot
5、wereusedtodetecttheexpressionanddistributionofSTAT3,phosphorylatedSTAT3(p-STAT3)andvascularendothelialgrowthfactor(VEGF);cellapoptosiswasdetectedbyTdT-mediateddUTP-biotinnickendlabeling(TUNEL)staining.ResultsIntheHIgroup,Thep-STAT3proteinsignificantlyincreasedat4
6、hours,reachedthepeakat6hours,begantodecreaseat8-12hours,whichweresignificanthigherthanthoseintheshamgroup(P﹤0.05).TherewasnosignificantdifferenceobservedwhencomparedtheexpressionoftotalSTAT3proteinintheHIgroupwiththoseoftheshamgroup.IntheHIgroup,theVEGFexpression
7、washigherthanthatintheshamgroupateachtimepoint.TUNELstainingshowedthatthepositivecellspeakedat24hours,andthepositivecellsweresignificantlymorethanthoseofshamgroup(P﹤0.01).ConclusionThep-STAT3proteinexpressionwassignificantlyincreasedafterHI,p-STAT3mayinduceVEGFex
8、pression,andinhibitneuronalapoptosisafterHI.Keywords:Signaltransducerandactivatoroftranscription;STAT3;VascularendothelialGrowthfactor;Apoptosis;Hypoxic-ischem
