中文摘要：

目的：通过腺病毒载体介导外源性KLF4在大鼠颈动脉球囊剥脱血管中进行表达，观察新生内膜增生情况，研究外源性KLF4对球囊损伤诱导的新生内膜形成的影响及初步探讨其机制。方法：构建含有KLF4基因的重组腺病毒载体pAd—KLF4，将其导入内皮剥脱的血管壁。用HE染色观察血管新生内膜的厚度，免疫组织化学染色和RT—PCR分别检测外源性KLF4在血管中的表达以及与增殖和分化标志基因表达的关系。结果：重组腺病毒pAd—KLF4可在血管壁中稳定表达KLF4。KLF4的过表达可显著抑制球囊损伤后血管新生内膜的增厚，转染pad—KLF4的血管，其内膜／中膜比值（I／M）（0．52±0．15）明显小于pad对照组（2．48±0．38），P〈0．05。pAd—KLF4组血管壁增殖标志蛋白PCNA和c—Jun表达也较pAd组明显降低（P〈0．05）。结论：KLF4过表达可阻断损伤诱导的血管平滑肌细胞表型转化，进而抑制球囊剥脱后血管内膜的增生。

英文摘要：

AIM： To observe the neointimal hyperplasia and to investigate the effect and mechanism of exogenous kruppel - like factor 4 （ KLF4 ） on neointimal formation induced by balloon injury. METHODS ： Adenovirus vector encoding the KLF4 （pAd -KLF4） was constructed and transfected into the balloon -injured carotid artery in rat. Neointima thickening was assessed using HE staining. Expression of exogenous KLF4 and the marker genes were detected by immunohistochemistry and RT - PCR. RESULTS： pad - KLF4 stably expressed KLF4 protein in the transfected vascular wall. Overexpression of KLF4 significantly inhibited neointimal hyperplasia induced by balloon injury. The ratio of intima - to - media area （I/M） in pAd - KLF4 group （2.48 ±0. 38） was significantly less than that in pad group （0. 52 ±0. 15） （ P 〈 0. 05 ）. Proliferating cell nuclear antigen （PCNA） and c - Jun were significantly reduced in pAd - KLF4 group, compared with the pad group （ P 〈 0. 05 ）. CONCLUSION： Overexpression of KLF4 inhibits the phenotype remodeling of vascular smooth muscle cells and neointimal hyperplasia induced by balloon injury.