摘要
目的研究体内转染eNOS(内皮型一氧化氮合酶)基因对损伤后血管内膜新生的抑制作用。方法2F球囊导管损伤大鼠颈总动脉内膜后,随机分成空白对照组、pcDNA3.1(-)组和pcDNA3.1-eNOS组,分别以PBS、脂质体Fugene6介导pcDNA3.1(-)和pcDNA3.1-eNOS体内转染至损伤后血管段,2周后对转染后血管平滑肌细胞行RT-PCR鉴定eNOS基因mRNA表达;转染1个月和2个月后对各组颈总动脉行免疫组化染色,计算机图像分析计算新生内膜面积(I)、新生内膜/中膜面积比值(I/M)。结果pcDNA3.1-eNOS体内转染组的颈总动脉血管平滑肌细胞有效表达eNOS基因mRNA。转染后1个月和2个月,eNOS基因体内转染组血管新生内膜面积、I/M比值均比PBS对照组、空载体pcDNA3.1(-)转染组显著减少(P<0.01)。结论eNOS基因体内转染损伤后动脉能有效抑制血管内膜新生,防止损伤后血管再狭窄。
Objective To study the inhibitional effect of endothelial nitric oxide synthase（eNOS） gene transfeetion on neointimal proliferation of artery after ballon injury. Methods An animal model of intimal stripping injury in wastar rat＇ s common carotid artery was established by 2F catheter. Then all these rats were divided into three groups randomly：blank control group with phosphate buffered saline （PBS） transfeetion to the injured vascular,peDNA3, 1（-）group and pcDNA3. 1-eNOS group which were transfeetd to the injured vasculars in vivo by PeDNA3.1 （-）vector and the recombinant PeDNA3. 1-eNOS vector respectively mediated by Fugene 6. Two weeks later, the transfected vasculars were obtained to detect expression of eNOS mRNA in cultured smooth muscle cells. 1 months and 2 months after transfection,immunochemical staining and computer image analysis system were employed to analyze the effects of eNOS transfection on neointimal proliferation thickness（I）and the ratio of neointimal-to -media（I/M）. Results The transfected common carotid arteries were confrrmd the mRNA expression of eNOS gene in cultured smooth muscle cells, 1 and 2 months after transfection, neointimal area and the ratio of meointimal-to-media （I/M）were significantly reduced in peDNA3.1-eNOS transfected group than PBS group or peDNA3.1 （-） transfeeted group（ P 〈 0.01 ）. Conclusion eNOS gene transfer to smooth muscle cells of injured artery in vivo might reduce arterial restenosis by inhibition of neointima proliferation.
出处
《四川医学》
CAS
2008年第11期1472-1474,共3页
Sichuan Medical Journal
关键词
一氧化氮合酶
基因治疗
体内转染
再狭窄
nitric oxide synthase
gene therapy
gene transfection in vivo
restenosis
