新生大鼠缺氧缺血脑损伤时脑组织stat3信号通路的作用

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1、新生大鼠缺氧缺血脑损伤时脑组织STAT3信号通路的作用邓睿1周立刚1赵凤艳2张莉2李德渊2母得志2（400013重庆，重庆市妇幼保健院新生儿科；610041四川成都，四川大学华西第二医院儿科2）[摘要]目的研究信号转导和转录激活因子3（STAT3）信号通路在新生大鼠缺氧缺血（HI）脑损伤中的作用。方法采用Rice法建立7日龄SD大鼠缺氧缺血脑损伤（HIBD）模型，同时设立对照。于HI后4h、6h、8h、12h和24h取脑，采用免疫组织化学法及Westernblot检测STAT3、磷酸化STAT3（p-STAT3）及血管内

2、皮生长因子（VEGF）的表达与分布，TUNEL法检测神经细胞凋亡。结果HI组p-STAT3蛋白表达在HI后4h升高，6h达高峰，8~12h逐渐下降，均明显高于假手术组，差异有统计学意义（P﹤0.05）。而STAT3总蛋白表达与假手术组比较，差异无统计学意义（P﹥0.05）。VEGF于HI后各时间点均明显高于假手术组，差异有统计学意义（P﹤0.05）。TUNEL染色阳性细胞数于HI后24h达高峰，明显高于假手术组，差异有统计学意义(P﹤0.01)。结论新生大鼠HI后，p-STAT3蛋白表达增高，可能诱导VEGF表达，对神经

3、元的凋亡具有抑制作用。[关键词]信号转导和转录激活因子；STAT3；血管内皮生长因子；凋亡；缺氧缺血性脑损伤；新生大鼠[中图分类号]R-72[文献标识码]A[文章编号]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