动脉内膜损伤及三种反义c-myc RNA的作用

Arterydenuded model and effects of threekinds of antisensec-myc RNA

目的 了解反义c myc基因导入对血管壁的影响。方法 将分别载有c myc第 1、2和 3外显子反义片段的三种重组逆转录病毒表达载体aM1、aM2和aM3导入球囊损伤的兔股动脉壁 ,并于术后 2 1天进行表达检测。结果 (1 )兔股动脉区域不仅利于控制损伤、给药和取材 ,而且血管内膜和中膜的面积比达到了 1 37∶1 ,其中膜c myc表达强度和面积增至正常的 1 8倍和 1 5倍 ;(2 )三个反义实验组中膜和内膜c myc表达则显著减少 ,其中aM2、aM3和aM1中膜强度分别减少了 37 5 %、2 0 8%和 1 7 8% ,面积分别减少了 71 5 %、5 7 2 %和 6 1 6 % ,内膜强度分别减少了 31 3%、2 0 8%和 1 7 8% ;(3)aM2组内膜 /中膜比下降了 72 6 % ,aM3组下降了 35 2 % ;(4)三种反义转染组内膜和中膜增殖细胞核抗原 (PCNA)表达出现强度增加而面积显著减少的现象 ;(5 )与内膜 /中膜比下降相平行 ,三个反义转染组中膜和内膜α SMactin的表达明显增加 ,增加程度为aM2 >aM3>aM1。结论 兔股动脉损伤模型可以取得满意的模型效果 ,而反义c myc导入能减少和抵消损伤血管myc的表达增加 ,对抗损伤所造成的血管壁内膜增生和平滑肌细胞去分化 ,并以aM2作用最强。

Objective Toinvestigatetheeffectsofantisensec myconinjuriedvascularwall Methods Threerecombinantretroviralexpressionvectors ,aM1 ,aM2andaM3,whichloadingthereversefragmentofexon1 , 2and 3respectively ,weretransferredintodenudedrabbitfemoralarterywallandwereassayed 2 1daysafter operation Results (1 )Theregionsofrabbitfemoralarterywerenotonlyconvenientforinjurycontrol,drug givingandmaterialdrawing ,butalsogaveaneointimalareatomediaareavatioof1 37∶1 Theirintensityandarea ofc mycexpressioninmediaincreasedto 1 8and 1 5foldofnormalvalue (2 )c mycexpressioninaM2 ,aM3 andaM1wasreducedby 37 5 % ,2 0 8% ,and 1 7 8%withmediaintensity ,71 5 % ,5 7 2 % ,and 6 1 6 %with mediaareaand 31 3% ,2 0 8% ,and 1 7 8%withneointimalintensityrespectively (3)Neointimalarea/media areaofaM2groupreducedby 72 6 % ,aM3groupreducedby 35 2 % ,aM1grouphadnosignificantdifference comparingwithcontrolgroup (4)Proliferatingcellularnuclearantigen (PCNA)intheintimalandmediaofthe threeantisensetransferredgroupswasenhancedwiththeirexpressiveintensities ,butreducedwithexpressiveareas significantly (5 )Withthedecliningofneointimalarea/mediaarea ,α SMactinexpressionintheintimaland mediaofthethreeantisensetransferredgroupswassignificantlyincreased (aM2 >aM3>aM1 ) Conclusion (1 ) Rabbitfemoralarterydenudedmodelisasatisfactoryanimalmodel (2 )Antisensec myctransferringcanreduce orresistthec mycincreaseininjuredarterywall,resistneointimalhyperplasiaandsmoothmusclecells dedifferentiation ,especiallyc mycexon 2antisenseRNAvectoraM2