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时间:2017-12-08
《靶向生存素sirna抑制人喉鳞癌裸鼠动物模型的实验研究》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、第47卷第3期哈尔滨医科大学学报Vo1.47,No.32122013年6月JOURNALOFHARBINMEDICALUNIVERSnYJun.,2013靶向生存素siRNA抑制人喉鳞癌裸鼠动物模型的实验研究王琳,郭岩,姚鸿超,肖辉,刘鸣(哈尔滨医科大学附属第二医院耳鼻咽喉一头颈外科,黑龙江哈尔滨150081)[摘要]目曲研究靶向生存素siRNA对喉鳞癌动物模型的抑制作用,探讨其可能的抑瘤机制。方法建立人喉鳞癌裸鼠移植瘤模型,将33只裸鼠随机分为3组,对照组瘤体内注射PBS液,空载体组瘤体内注射空慢病毒载
2、体(Ad.contro1),治疗组应用生存素siRNA(Ad—survivin)进行瘤内注射治疗,观察各组肿瘤生长情况,光镜及透射电镜观察肿瘤超微结构变化,TUNEL法检测细胞凋亡,免疫组化法检测Bcl-2蛋白的表达情况。结果治疗组体内注射生存素siRNA(100ng·mL~·d),裸鼠肿瘤生长受到明显抑制,与对照组及空载体组相比,差异有统计学意义(P<0.05)。光镜、电镜下观察到治疗组肿瘤组织发生坏死和凋亡改变,Tunel证实治疗组肿瘤细胞凋亡数目明显增多,与对照组及空慢病毒组相比,差异有统计学意义(
3、P4、IUMing(DepartmentofOtolaryngology—Head&ⅣeSurgery,TheSecondAffiliatedHospitalofHarbinMedicalUniversity,Harbin150081,China)Abstract:ObjectiveToinvestigatethetherapeuticeffectofsurvivinsiRNA,relatedarres-tant—inducingonhumanlaryngealsquamouscarcinomainnudemi5、ce,andtoexplorethepossi—blemechanism.MethodsNudemousemodelbearinglaryngocarcinomawasestablishedbyU—singhumanlaryngealsquamouscarcinomacellline(Hep-2).Thirty—threemicewererandomlydividedintothreegroups:thecontrolgroupintratumoralinjectionofPBS,emptyvectorg6、roupintratumoralinjectionofemptylentiviralvector(Ad—contro1),andthetreatmentgroupwasgiv-ensurvivinsiRNA.Tumorgrowthandthetumormicroscopicstructurechangeswereobservedwithlightmicroscopyandtransmissionelectronmicroscopy.TUNELwasusedtodetecttheap—optosiscell7、sincontrolgroupandtreatmentgroup.ImmunohistochemicaltechniquewasusedtoexaminetheexpressionofBcl-2protein.Results/nvivo,tumorgrowthwassignificantlyin—hibitedintreatmentgroupcomparedtothecontrolgroupandemptyvectorgroup,thedifferencewasstatisticallysignifica8、nt(P<0.05).Thenecrosisandapoptosisofthetumorcellswerefoundunderlightandelectronmicroscope.TheTunnelshowedcellapoptosiswasobviousintreatmentgroup,andBcl·2expressionwasobviouslyinhibitedinimmunohistochemistry.[收稿日期]2o
4、IUMing(DepartmentofOtolaryngology—Head&ⅣeSurgery,TheSecondAffiliatedHospitalofHarbinMedicalUniversity,Harbin150081,China)Abstract:ObjectiveToinvestigatethetherapeuticeffectofsurvivinsiRNA,relatedarres-tant—inducingonhumanlaryngealsquamouscarcinomainnudemi
5、ce,andtoexplorethepossi—blemechanism.MethodsNudemousemodelbearinglaryngocarcinomawasestablishedbyU—singhumanlaryngealsquamouscarcinomacellline(Hep-2).Thirty—threemicewererandomlydividedintothreegroups:thecontrolgroupintratumoralinjectionofPBS,emptyvectorg
6、roupintratumoralinjectionofemptylentiviralvector(Ad—contro1),andthetreatmentgroupwasgiv-ensurvivinsiRNA.Tumorgrowthandthetumormicroscopicstructurechangeswereobservedwithlightmicroscopyandtransmissionelectronmicroscopy.TUNELwasusedtodetecttheap—optosiscell
7、sincontrolgroupandtreatmentgroup.ImmunohistochemicaltechniquewasusedtoexaminetheexpressionofBcl-2protein.Results/nvivo,tumorgrowthwassignificantlyin—hibitedintreatmentgroupcomparedtothecontrolgroupandemptyvectorgroup,thedifferencewasstatisticallysignifica
8、nt(P<0.05).Thenecrosisandapoptosisofthetumorcellswerefoundunderlightandelectronmicroscope.TheTunnelshowedcellapoptosiswasobviousintreatmentgroup,andBcl·2expressionwasobviouslyinhibitedinimmunohistochemistry.[收稿日期]2o
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