野生型p53基因转移对血管内膜损伤后再狭窄的防治作用

Prevention and treatment of restenosis after endangium injury by using wild p53 genetransfer

为防止血管成形术后管腔再狭窄，我们构建了介导野生型ｐ５３基因转移的复制缺陷型重组腺病毒（Ａｄ－ｐ５３），将Ａｄ－ｐ５３感染日本大耳兔球囊损伤后的髂动脉，并通过携带ＬａｃＺ基因重组腺病毒感染观察基因转染效率。结果可见Ａｄ－ｌａｃＺ感染损伤后的动脉３天后血管内膜、中膜、外膜均有ＬａｃＺ基因的阳性表达；Ａｄ－ｐ５３感染损伤后的髂动脉２周后可见血管内膜增厚程度、内膜与中膜的比例明显减小，管腔狭窄程度明显减轻，ｐ５３蛋白大量表达，与对照组相比具有显著差异。证明野生型ｐ５３基因转移能明显抑制血管损伤后的内膜增殖，为野生型ｐ５３基因转移防治血管内膜损伤后再狭窄奠定了实验基础。

To prevent the process of restenosis after arterial injury,we constructed a replication defective adenovirus encoding wild type p53 gene by homologous recombination.In vivo studies,balloon injured rabbits's iliac segments were infected by Ad p53 and Ad lacz.The gene transfection efficiency was tested by x gal staining.The results showed that in vivo adenovirus vectors had high transferring efficiency by x gal staining.In the group treated by Ad p53,the thickening degree of initima and I/M greatly decreased,and p53 protein largely expressed after injuring 3 weeks.Our study demonstrated that wild type p53 genetransfer could greatly inhibit proliferation of arterial intima after balloon injury and this paper provided the experimental evidences for preventing arterial restenosis.