P53病毒增强型质粒-脂质体复合物对血管平滑肌细胞增殖的抑制作用

目的:研究腺相关病毒增强型质粒载体介导的p53基因对血管平滑肌细胞（VSMC）的作用，探讨其用于防治冠状动脉旁路术后移植血管再狭窄等心血管内外科疾病的可能性。方法：构建了野生型p53基因的腺相关病毒增强型质粒表达载体，通过阳离子脂质体Dosper介导，体外转染杂VSMC。聚合酶链技术检测的基因表达。应用细胞计数及DNA合成分析技术,测定p53基因对VSMC增殖的抑制效应。结果：外源性p53基因可有效导入VSMC并表达；p53基因导入可显著抑制细胞生长，DNA合成减少。结论：野生型p53基因腺相关病毒增强型质粒载体转染VSMC可有效地抑制细胞增殖。

Inhibition of Vascular Smooth Cell Proliferation with Transfer of Wild -type p53 Gene Using a Vector Based on Adeno-associated Virus Plasmid

Objective:To study the effect of extrinsic wild type p53 gene mediated by adenoassociated virus plasmid vector on vascular smooth muscle cells(SMCs) and the possibility of p53 gene therapy for vessel graft restenosis after coronary artery bypass.Methods:Human wild type p53 gene adeno associated virus plasmid vector was constructed and transfected into rabbit vascular SMCs mediated by the cationic liposome Dosper in vitro.The gene expression was determined by polymerase chain reaction technique.Proliferation of SMCs was investigated by cell counting and isotope incorporation.Results:The extrinsic wild type p53 gene was effectively transferred into the cells with adeno associated virus plasmid vector.The overexpression of p53 gene restricted the proliferation of SMCs and decreased the DNA synthesis.Conclusion:The constructed p53 adeno associated virus plasmid may play a role in gene prevention of vessel graft restenosis after coronary artery bypass.