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探讨重组 2型腺相关病毒载体介导 2型成纤维细胞生长因子基因诱导家兔缺血心肌血管生成的作用。实验对象为 2 0只新西兰兔 ,手术建立心肌缺血模型后随机分为成纤维细胞生长因子基因治疗组和对照组 ,分别向缺血区域心肌注射成纤维细胞生长因子腺相关病毒或磷酸盐缓冲液。 4周后取心肌及肝、肾等器官组织标本 ,采用逆转录聚合酶链反应检测目的基因mRNA的表达 ;制作组织学切片以观察组织病理改变 ,于高倍镜下计数缺血区域微血管数目。结果发现转染的 2型成纤维细胞生长因子基因在缺血心肌中有表达 ,成纤维细胞生长因子基因治疗组缺血区域单个高倍视野内的微血管数为 12 .0± 1.4条 ,对照组为 4 .5± 1.5条 ,二者差异具有显著性 (P <0 .0 1)。 2型成纤维细胞生长因子基因治疗组的肝脏、肾脏、脾脏、角膜和睾丸标本中均未发现 2型成纤维细胞生长因子基因的表达 ,病理检查也未发现组织结构异常。说明腺相关病毒载体介导的 2型成纤维细胞生长因子基因可以有效地转染入家兔缺血心肌 ,并具有明显的诱导缺血心肌血管生成的作用 ,且基因表达仅限于心肌。
To investigate the effect of recombinant adenovirus-2 (AAV-2) on inducing angiogenesis in rabbits with ischemic myocardium mediated by type 2 fibroblast growth factor gene. The experimental group was 20 New Zealand rabbits. After establishment of myocardial ischemia model, they were randomly divided into fibroblast growth factor gene therapy group and control group, respectively, to the ischemic area of myocardial injection of fibroblast growth factor adeno-associated virus or phosphate buffered saline liquid. After 4 weeks, samples of heart, liver, kidney and other organs and tissues were collected. Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the mRNA expression of the target gene. Histological sections were made to observe histopathological changes and count the number of microvessels in ischemic area under high magnification. The results showed that the transfected type 2 fibroblast growth factor gene was expressed in ischemic myocardium. The number of microvessels in single high power field in the ischemic area of fibroblast growth factor gene therapy group was 12 ± 0. 4, while the control group was 4.5 ± 1.5, the difference was significant (P <0.01). Type 2 fibroblast growth factor gene therapy group liver, kidney, spleen, cornea and testicular specimens were not found in type 2 fibroblast growth factor gene expression, histopathological examination also found no structural abnormalities. These results suggest that adeno-associated virus vector-mediated gene expression of type 2 fibroblast growth factor can be efficiently transfected into ischemic myocardium of rabbits and have obvious effects on inducing ischemic myocardial angiogenesis. Gene expression is limited to myocardium.