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时间:2020-05-20
《雷公藤甲素对支气管哮喘小鼠STAT-1与ICAM-1表达的影响-论文.pdf》由会员上传分享,免费在线阅读,更多相关内容在行业资料-天天文库。
1、国际呼吸杂志2014年7月第34卷第13期IntJRespir,July2014,Vo1.34,No.13·96l·.论著雷公藤甲素对支气管哮喘小鼠STAT一1与ICAM一1表达的影响张朝顺何建猷冯起校覃善君【摘要】目的研究雷公藤甲素对支气管哮喘(简称哮喘)小鼠肺组织中信号转导和转录激活因子一1(STAT一1)与细胞间黏附分子一1(ICAM一1)表达的影响,探讨其治疗哮喘的机制。方法4O只雄性昆明小鼠随机分成4组:正常对照组、哮喘组、地塞米松治疗组及雷公藤甲素治疗组,以卯清蛋白致敏和激发方法建立哮喘小鼠动物模型并给予相应治
2、疗。24d后处死小鼠,检测BALF中自细胞总数及嗜酸粒细胞(EOs)计数;采用逆转录一聚合酶链反应(RT-PCR)方法检测肺组织中STAT一1、ICAM一1mRNA表达水平;采用免疫组织化学法检测肺组织中STAT-1、ICAM一1蛋白表达水平。结果哮喘组STAT-1、ICAM一1mRNA及蛋白表达明显高于正常对照组(P<0.01),雷公藤甲素治疗组及地塞米松组明显低于哮喘组(P3、677,P<0.01)。肺组织ICAM一1蛋白表达与白细胞总数、EOS计数呈正相关(r分别为0.792,0.776,Pd0.01)。结论雷公藤甲素抑制哮喘气道炎症的机制可能与其抑制STAT一1与ICAM-1的表达活性有关。【关键词】支气管哮喘;雷公藤甲素;信号转导和转录激活因子一1;细胞间黏附分子一1EffectsoftriptolideontheexpressionofSTAT-1andICAM’1inasthmaticmiceZhangChaoshun,HeJianyou,FengQixiao,QinShanjun.R4、espiratoryDiseaseResearchInstituteofGuangdongMedicalCollege,Zhanjiang524001,ChinaCorrespondingauthor:HeJianyou,Email:ngcs790622@163.corn[Abstract]ObjectiveTostudytheeffectsoftriptolideontheexpressionofSTAT+,1andICAM—。1inasthmaticmice,andtoexplorethepossibletherape5、uticmechanismoftriptolideinasthma.MethodsFortyKunmingmalemicewererandomlydividedinto4groups:controlgroup,asthmaticgroup,dexamethasonegroupandtriptolidegroup.Theasthmaticmodelwasestablishedbyovalbumininjectionandihalation.Andthe4groupsweretreatedrespectivelywithnor6、malsaline(ascontro1),dexamethasoneortriptolide.Twenty—fourdayslater,themicewereexecuted.Thenumbersoftotalleukocytesandeosinophilsinbronchoalveolarlavagefluid(BALF)werecountedbyopticalmicroscope.RT—PCRwasemployedtodetectthemRNAofSTAT一1andICAM一1inthelungtissue.Thepr7、oteinofSTAT一1andICAM一1expressionweremeasuredbyimmunohistochemistry.ResultsSTAT一1andICAM一1mRNAandtheproteinexpressioninlungtissueofasthmaticgroupsignificantlyincreasedcomparedwiththoseofcontrolgroup(Pd0.01).ThemRNAandproteinexpressionofSTAT一1andICAM一1inmicetreatedw8、ithtriptolideanddexamethasoneweresignificantlylowerthanthoseinasthmaticgroup(P<0.01).STAT一1proteinexpressioninlungtissuewascorrelatedwiththenumberoftota
3、677,P<0.01)。肺组织ICAM一1蛋白表达与白细胞总数、EOS计数呈正相关(r分别为0.792,0.776,Pd0.01)。结论雷公藤甲素抑制哮喘气道炎症的机制可能与其抑制STAT一1与ICAM-1的表达活性有关。【关键词】支气管哮喘;雷公藤甲素;信号转导和转录激活因子一1;细胞间黏附分子一1EffectsoftriptolideontheexpressionofSTAT-1andICAM’1inasthmaticmiceZhangChaoshun,HeJianyou,FengQixiao,QinShanjun.R
4、espiratoryDiseaseResearchInstituteofGuangdongMedicalCollege,Zhanjiang524001,ChinaCorrespondingauthor:HeJianyou,Email:ngcs790622@163.corn[Abstract]ObjectiveTostudytheeffectsoftriptolideontheexpressionofSTAT+,1andICAM—。1inasthmaticmice,andtoexplorethepossibletherape
5、uticmechanismoftriptolideinasthma.MethodsFortyKunmingmalemicewererandomlydividedinto4groups:controlgroup,asthmaticgroup,dexamethasonegroupandtriptolidegroup.Theasthmaticmodelwasestablishedbyovalbumininjectionandihalation.Andthe4groupsweretreatedrespectivelywithnor
6、malsaline(ascontro1),dexamethasoneortriptolide.Twenty—fourdayslater,themicewereexecuted.Thenumbersoftotalleukocytesandeosinophilsinbronchoalveolarlavagefluid(BALF)werecountedbyopticalmicroscope.RT—PCRwasemployedtodetectthemRNAofSTAT一1andICAM一1inthelungtissue.Thepr
7、oteinofSTAT一1andICAM一1expressionweremeasuredbyimmunohistochemistry.ResultsSTAT一1andICAM一1mRNAandtheproteinexpressioninlungtissueofasthmaticgroupsignificantlyincreasedcomparedwiththoseofcontrolgroup(Pd0.01).ThemRNAandproteinexpressionofSTAT一1andICAM一1inmicetreatedw
8、ithtriptolideanddexamethasoneweresignificantlylowerthanthoseinasthmaticgroup(P<0.01).STAT一1proteinexpressioninlungtissuewascorrelatedwiththenumberoftota
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