吡格列酮對(duì)大鼠心肌缺血再灌注損傷中炎癥反應(yīng)及細(xì)胞凋亡的影響

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1、ltainanMedJ，Dec．2013，Vo1．24，No．24海南醫(yī)學(xué)2013年l2月第24卷第24期doi：10．3969／j．issn．1003—6350．2013．24．1495吡格列酮對(duì)大鼠心肌缺血再灌注損傷中炎癥反應(yīng)及細(xì)胞凋亡的影響李鳳云。，楊鳳蘭’，張秀萍，劉志明f1．秦皇島市撫寧縣人民醫(yī)院心內(nèi)科，河北秦皇島066300；2．廣西醫(yī)科大學(xué)附屬第一醫(yī)院心內(nèi)科，廣西南寧530000)【摘要】目的探討吡格列酮對(duì)大鼠心肌缺血再灌注損傷中炎癥反應(yīng)和細(xì)胞凋亡的影響及其機(jī)制。方法將80只SD大鼠隨機(jī)分為假手術(shù)組、模型組、吡格列酮組、GW9662組及DMSO組，每組

2、各l6只，術(shù)前5d分別給予相應(yīng)處理。采取體內(nèi)結(jié)扎左前降支的方法建立心肌缺血再灌注損傷模型，予ELISA法檢測(cè)大鼠心肌組織中NF--r．Bp65及IFN—估量水平，HE染色觀察左心室前壁細(xì)胞病理形態(tài)學(xué)改變，并采用原位末端標(biāo)記法檢測(cè)心肌細(xì)胞凋亡數(shù)。結(jié)果與假手術(shù)組相比，其余四組大鼠心肌組織中NF一1cEIp65及IFN1含量水平、心肌細(xì)胞凋亡數(shù)均顯著升高(P<0．05)；與模型組比較，吡格列酮組大鼠心肌組織中NF—r．Bp65及IFN_丫含量水平，心肌細(xì)胞凋亡數(shù)明顯降低(P．，0．05)；模型組與吡格列酮組中NF—r．Bp65及IFN-丫含量水平均呈顯著正相關(guān)(P

3、01)。結(jié)論吡格列酮在心肌缺血再灌注損傷中可能通過負(fù)性調(diào)節(jié)NF-rBp65含量水平進(jìn)而減少IFN_丫的釋放，抑制心肌細(xì)胞的凋亡，從而發(fā)揮相應(yīng)的心肌保護(hù)作用?！娟P(guān)鍵詞】吡格列酮；GW9662；心肌缺血／再灌注；炎癥反應(yīng)；細(xì)胞凋亡【中圖分類號(hào)】R-332【文獻(xiàn)標(biāo)識(shí)碼】A【文章編號(hào)】1003----6350(2013)24—3595—o4Efectofpioglitazoneoninflammatoryreactionandapoptosisofmyocardiumcellfromischemia-reperfusioninjuryinrats．L1Feng-yunl，Y

4、ANGFeng-lan，ZHANGXiu-ping29LIUZhi-ming2．1．DepartmentofCardiology,FuningCountryHospital,Qinhuangdao066300,Hebei,CHINA；2．DepartmentofCardiology,theFirstAffiliatedHospitalofGuangxiMedicalUniversity,Nanning530000,Guangxi，CHINA【Abstract】ObjectiveToinvestigatetheefectofpioglitazoneoninflamma

5、toryreactionandapoptosisofneuronsfollowingmyocardiumfromischemia-reperfusioninjuryinratsanditscorrespondingmechanisms．MethodsEightySprague—Dawleyratswererandomlydividedintofivegroupsassham·operationgroup，modelgroup，pioglitazonegroup，GW9662groupandDMSOgroup，with16ratsineachgroup．Relevan

6、ttreatmentsweregiventorats5daysbeforemyocardiumischemiaoperationrespecfivel~Aratmodelofleftanteriordescendingcoro-naryarterywasligatedfor45minandreperfusedfor45mintoestablishthemodelofischemia-reperfusion．ELISAWasrespectivelyusedtodetectlevelsofNF--KBp65andIFN—vinmyocardiumtissue．H．Est

7、ainingWasemployedtoobservemorphologicchangesofmyoeardiumcellsinischemia／reperfusioninjuryregion，andTUNELstainingwereusedtodetectthenumberofmyoeardiumcellapoptosis．ResultsComparedwithsham—operationgroup，thelevelsofNF--KBp65andIFN1，thenumberofmyocardiumcellapoptosisweresignificantlyinc