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时间:2017-12-08
《吡格列酮对大鼠心肌缺血再灌注损伤中炎症反应及细胞凋亡的影响》由会员上传分享,免费在线阅读,更多相关内容在学术论文-天天文库。
1、ltainanMedJ,Dec.2013,Vo1.24,No.24海南医学2013年l2月第24卷第24期doi:10.3969/j.issn.1003—6350.2013.24.1495吡格列酮对大鼠心肌缺血再灌注损伤中炎症反应及细胞凋亡的影响李凤云。,杨凤兰’,张秀萍,刘志明f1.秦皇岛市抚宁县人民医院心内科,河北秦皇岛066300;2.广西医科大学附属第一医院心内科,广西南宁530000)【摘要】目的探讨吡格列酮对大鼠心肌缺血再灌注损伤中炎症反应和细胞凋亡的影响及其机制。方法将80只SD大鼠随机分为假手术组、模型组、吡格列酮组、GW9662组及DMSO组,每组
2、各l6只,术前5d分别给予相应处理。采取体内结扎左前降支的方法建立心肌缺血再灌注损伤模型,予ELISA法检测大鼠心肌组织中NF--r.Bp65及IFN—估量水平,HE染色观察左心室前壁细胞病理形态学改变,并采用原位末端标记法检测心肌细胞凋亡数。结果与假手术组相比,其余四组大鼠心肌组织中NF一1cEIp65及IFN1含量水平、心肌细胞凋亡数均显著升高(P<0.05);与模型组比较,吡格列酮组大鼠心肌组织中NF—r.Bp65及IFN_丫含量水平,心肌细胞凋亡数明显降低(P.,0.05);模型组与吡格列酮组中NF—r.Bp65及IFN-丫含量水平均呈显著正相关(P3、01)。结论吡格列酮在心肌缺血再灌注损伤中可能通过负性调节NF-rBp65含量水平进而减少IFN_丫的释放,抑制心肌细胞的凋亡,从而发挥相应的心肌保护作用。【关键词】吡格列酮;GW9662;心肌缺血/再灌注;炎症反应;细胞凋亡【中图分类号】R-332【文献标识码】A【文章编号】1003----6350(2013)24—3595—o4Efectofpioglitazoneoninflammatoryreactionandapoptosisofmyocardiumcellfromischemia-reperfusioninjuryinrats.L1Feng-yunl,Y4、ANGFeng-lan,ZHANGXiu-ping29LIUZhi-ming2.1.DepartmentofCardiology,FuningCountryHospital,Qinhuangdao066300,Hebei,CHINA;2.DepartmentofCardiology,theFirstAffiliatedHospitalofGuangxiMedicalUniversity,Nanning530000,Guangxi,CHINA【Abstract】ObjectiveToinvestigatetheefectofpioglitazoneoninflamma5、toryreactionandapoptosisofneuronsfollowingmyocardiumfromischemia-reperfusioninjuryinratsanditscorrespondingmechanisms.MethodsEightySprague—Dawleyratswererandomlydividedintofivegroupsassham·operationgroup,modelgroup,pioglitazonegroup,GW9662groupandDMSOgroup,with16ratsineachgroup.Relevan6、ttreatmentsweregiventorats5daysbeforemyocardiumischemiaoperationrespecfivel~Aratmodelofleftanteriordescendingcoro-naryarterywasligatedfor45minandreperfusedfor45mintoestablishthemodelofischemia-reperfusion.ELISAWasrespectivelyusedtodetectlevelsofNF--KBp65andIFN—vinmyocardiumtissue.H.Est7、ainingWasemployedtoobservemorphologicchangesofmyoeardiumcellsinischemia/reperfusioninjuryregion,andTUNELstainingwereusedtodetectthenumberofmyoeardiumcellapoptosis.ResultsComparedwithsham—operationgroup,thelevelsofNF--KBp65andIFN1,thenumberofmyocardiumcellapoptosisweresignificantlyinc
3、01)。结论吡格列酮在心肌缺血再灌注损伤中可能通过负性调节NF-rBp65含量水平进而减少IFN_丫的释放,抑制心肌细胞的凋亡,从而发挥相应的心肌保护作用。【关键词】吡格列酮;GW9662;心肌缺血/再灌注;炎症反应;细胞凋亡【中图分类号】R-332【文献标识码】A【文章编号】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
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