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《银杏叶提取物诱导血红素氧合酶1表达抗缺血再灌注损伤后心肌细胞凋亡的研究》由会员上传分享，免费在线阅读，更多相关内容在应用文档-天天文库。
1、银杏叶提取物诱导血红素氧合酶-1表达抗缺血再灌注损伤后心肌细胞凋亡的研究【关键词】银杏叶提取物；,,血红素氧合酶-1；,,再灌注损伤；,,凋亡 摘要：目的探讨银杏叶提取物（EGb761）诱导血红素氧合酶-1（HO-1）表达抗缺血再灌注损伤（IRI）后心肌细胞凋亡的效果及其机理。方法48只兔随机均分为单纯IRI组、EGb761组、EGb761+ZnPPⅨ组，分别预先给予等容积的生理盐水，EGb761，EGb761+ZnPPⅨ腹腔内注入。24h后，每组任选8只处死，检测心肌细胞内HO-1表达及活性，余兔结扎冠脉左前降支使心肌缺血40min，再灌注4h，取缺血心肌检测中性粒细胞浸润、丙二醛（
2、MDA）含量、Bax蛋白与Bcl-2蛋白表达及心肌细胞凋亡指数（AI）。结果与单纯IRI组及EGb761+ZnPPⅨ组比较，EGb761组HO-1表达及活性均明显升高，中性粒细胞浸润及MDA含量明显降低，Bax增加而Bcl-2降低，心肌细胞AI显著减少(均为P<0.01)。与单纯IRI组比较，EGb761+ZnPPⅨ组HO-1表达增加但活性降低(P<0.05)，MDA含量明显升高(P<0.05)，其余指标均无显著差异。结论EGb761能明显诱导心肌细胞内HO-1表达，并通过HO-1的抗炎、抗氧化等作用下调Bax表达，上调Bcl-2表达，从而显著抑制IR损伤后心肌细胞凋亡
3、。 关键词：银杏叶提取物；血红素氧合酶-1；再灌注损伤；11凋亡 Abstract：ObjectiveToexploretheprotectiveeffectsandmechanismofhemeoxygenase-1(HO-1)expressioninducedbyextractofGinkgobiloba(EGb761)againstcardiomyocyteapoptosisfromischemiareperfusioninjury(IRI).Methods48rabbitswererandomlydividedintosimpleIRgroup,EGb761groupandE
4、Gb761+ZnPPⅨgroup.Eachrabbitindifferentgroupswasintraperitonealinjectedwithsaline(5ml),EGb761(10mg/kg),EGb761(10mg/kg)+ZnPPⅨ(7.5mg/kg)respectively.24hourslater,8rabbitsineachgroupwerekilledtomeasuremyocardialHO-1expressionandHO-1activity.Otherrabbitsweresubjectedfor40minofmyocardialischemiabyligat
5、ionofleftanteriordescendingcoronaryarteryfollowedby4hofreperfusion.Theneutrophilinfiltration,myocardialmalonaldehyde(MDA)content,BaxandBcl-2proteinexpression,cardiomyocyteapoptosisindex(AI)inischemiaareasweredetected.ResultsCamparedwithsimpleIRIgroupandEGb761+ZnPPⅨgroup,theexpressionandactivityof
6、myocardialHO-1increasedsignificantly,theneutrophilinfiltrationandMDAcontentdecreased.BaxexpressionincreasedandAIandBcl-2leveldecreasedinEGb761group(P<0.01respectively).ComparedwithsimpleIRIgroup,11EGb761+ZnPPⅨgroupshowedhighermyocardialHO-1expressionbutlowerHO-1activity(P<0.01),whiletheMDAc
7、ontentincreased(P<0.05),buttheneutrophilinfiltration,BaxandBcl-2expressionandAIshowednosignificantdifference.ConclusionEGb761couldinduceHO-1overexpression,throughitsantiinflammatoryandantioxidativeactiontoupregulate
