山楂叶总黄酮抑制慢性脑缺血模型大鼠脑组织神经元的凋亡.pdf

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1、中国组织工程研究第78眷第492014—11—30出版ChineseJournalofTissueEngineeringResea~hNovember30,2014Vo1．18,No．49WWW．CRTER．orgTotaIFlavoneofHan一OrnL■eaTiim■In一n■laD●It●SneUrona■IapoptosisinbraintissueofratmodelsofchroniccerebralischemiaTanRong·fang，XiaAi—hua，WuXiao-guang，CaoNa-na，LiMeng·meng，ZhangTian-ge，Wan

2、gYi·ru，YueZhi-lingInstituteofBasicMedicine，ChengdeMedicalColege，Chengde067000,HebeiProvince，ChinaAbstractBACKGR0UND：Cerebrovasculardiseaseoftencausesdysfunctionoflhebrainnerve．andnervecelTanRong·fang．Instituteofapoptosisistheimportantfactorofcerebralnervedysfunction．Theexcessiveexpressiono

3、fC-foScanblocktheBasicMedicine，Chengdetransductionofintracellularsignalsothatproducingsomeapoptosis—promotingfactors，whichinvolveinnerveMedicalColege，Chengde067000，HebeiProvince，cellapoptosisprocessafterischemiainjuryofbrain．Bcl-2isaninhibitedfactor．ItmighttobethekeytotreatChinaischemiccer

4、ebrovasculardiseasebyinhibitingorreducingtheapoptosisofnervecellsafterischemiainjury．OBJECTIVE：ToinvestigatethetherapeuticefectandmechanismoftheTotalFlavoneofHawthornLeafonCorrespondingauthor：Wuchroniccerebralischemiarats．Xiao—guang，Master．METHODS：Atotalof72healthymaleSprague—Dawleyratswer

5、erandomlydividedintoshamsurgerygroup，Associateresearcher,modelgroup，TotalFlavoneofHawthornLeafgroupandginkgoleafgroup．PermanentbilateralcarotidarterylnstituteofBasicMedicinefigationwasusedtopreparechroniccerebralischemiamodelinthemodeIgroup．TotalFlavoneofHawthornChengdeMedicalCollege，Leafg

6、roupandginkgoleafgroup．TotalFlavoneofHawthornLeafgroupandginkgoleafgrouprespectivelyChengde067000，Hebeireceived140mg／kgTotalFlavoneofHawthornLeafand12．3mg／kgginkgoleafintragastricallyfor36daysfrOmProvinceChina36daysaftermodelinduction．Modelgroupandshamsurgerygroupreceived3．5mUkgphysiologic

7、alsalinedoi：l03969rj．issn20954344intragastrically．201449002RESULTSANDCONCLUSlON：Comparedwiththemodelgroup．theexpressionofc-fosproteinsignificantly【http：／Avwwcrter．org】deceasedintheTotaIFlavoneofHawthornLeafgroup(P<0．01)，Bcl一2expressionIevelssignificantlyjncrea