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1、XX大学毕业论文胸昔激酶系统血管靶向抗肝癌效应的机制姓名：2014年6月25日作者：李宝金，张超，周玉梅，郝颖，刘晓平，区庆嘉【关键词】肝肿瘤；KDR启动子；基因治疗;重组腺病毒；胸昔激酶系统；HepG2细胞；裸鼠,Balb/c[Abstract]AIM:ToexplorethetherapeuticefficacyandmechanismofHSVtkfortargetingangiogenesisagainsthepatocellularcarcinoma.METHODS:ByusingpAdeasysystem,recombinantadenoviruscontainingkinase
2、domainreceptor(KDR)orcytomegalovirus(CMV)promotercontrolledHSVtkgene(AdKDRtkandAdCMVtk)wasconstructed.TheviruswasusedtoinfectKDRexpressedhumanumbilicalvenousendothelialcells(HUVEC)andKDRunexpressedHepG2.Followingadministrationofganciclovir(GCV),thesurvivalrateofgenetransfectedHUVECandHepG2wasevalua
3、tedbyusingMTTmethod.Hepatocarcinomasweretransplantedin32Balb/cmicewithHepG2cells,whichweresubsequentlydividedinto4groups:GCVgroup(1),Adgroup(II),AdCMVtkgroup(III)andAdKDRtkgroup(IV).ThenselectiveadministrationofrecombinantadenovirusorAdintratumorallywasperformedinallrats.GCVwasgivenatadoseof100mg/(
4、kgd)ipinthefollowingdaysandfor10d.Microvesseldensity(MVD)oftumorinallthetreatedanimalswascheckedwiththeimmunohistochemicalmethodsandtumorburdenwasassessed10dbeforeandafterthelastGCVadministration.RESULTS:ThepAdeasysystemproducedahightiteroftherecombinantadenovirus[(1x1013)pfu/L]•Whenthemultiplicity
5、ofinfection(MOI)was100,withincreasingGCVconcentrationfrom0upto50mg/L,thesurvivalrateofAdKDRtktransfectedHUVECandHepG2decreasedfrom(90.7±4.5)%and(91.8±4.3)%to(2&9±5.7)%and(75.4±2.9)%,respectively(P0.01),whilethesurvivalrateofAdCMVtktransfectedHUVECandHepG2declinedfrom100%to(17.6±2.5)%and(23.2±5.7)%,
6、respectively(P0.05).ComparedwithgroupI.therewasadecreaseoftumorweightby(14.7±3.2)%ingroupIIIand(23.6±5.6)%ingroupIV,respectively;andtherewasadistinctdifferencebetweengroupIIIandIV(P0.05).ThemedianMVDwas37.4±8.6,30.6±7・8,27・6±7・1,10・7±4.1(microvessels/mm2)ingroupI,II,IIIandIV,respectively;andtherewe
7、resignificentdifferencesbetweengroupIIIandII(P0.05),IVandII(P0.01),IVandIII(P0.01).CONCLUSION:KDRpromoterHSVtkgenemayeffectuallyrestrainthegrowthoftumorviatargetingangiogenesisofhepatocellularcarcinomawitht
