论文部分内容阅读
探讨血管内皮细胞的特异丝裂原 -血管内皮生长因子 (VEGF)基因阻止血管内膜损伤后形成再狭窄的组织变化过程。建立球囊拉伤血管内膜的兔髂动脉模型 ,将携带 VEGF目的基因的真核表达载体 pc DNA3/ VEGF经多聚赖氨酸处理的PTCA球囊导管导入拉伤的血管内膜。 VEGF基因组拉伤 2周时血管内壁有 VEGF m RNA和蛋白的高表达。血管内膜内皮化较快。 2周时即有许多血管内皮细胞呈岛状分布。 4周时内膜基本恢复光滑。内膜平滑肌细胞增生明显减少。而对照组 2周时血管内膜粗糙 ,基底膜暴露 ,拉伤后 4周仍无内皮细胞再生 ,最后形成虫蚀样改变。血管中膜平滑肌细胞穿过内弹性膜进入内膜并大量增生 ,内膜增厚。VEGF基因定位导入血管内壁后 ,VEGF m RNA和蛋白高表达且发挥其生物学效应 ,内皮细胞岛状增生 ,加快内膜内皮化 ,减轻内膜增厚
To investigate the histopathological changes of vascular endothelial cell-specific mitogen-vascular endothelial growth factor (VEGF) gene to prevent restenosis after vascular intimal injury. Rabbit iliac arteries of balloon-intima were established. The eukaryotic expression vector pcDNA3 / VEGF carrying VEGF gene was introduced into the injured intima by PTCA balloon catheter. The VEGF mRNA and protein were highly expressed in the vascular wall at 2 weeks after injury in the VEGF genome. Intimal endothelialization faster. At 2 weeks, many vascular endothelial cells showed island-like distribution. At 4 weeks, the basic recovery of endometrial smooth. Intimal smooth muscle cell proliferation was significantly reduced. The control group at 2 weeks when the intima of the rough, basement membrane exposure, 4 weeks after injury still no endothelial cell regeneration, the final formation of worm-eaten samples change. Vascular tunica media smooth muscle cells enter the intima through the inner elastic membrane and proliferate in a large amount, the intima is thickened. VEGF gene localization into the vascular wall, VEGF m RNA and protein expression and exert its biological effects, endothelial island proliferation, accelerate endothelialization, reduce intimal thickening