Chen L, Guo J, Guo J
Fuwai Hospital, Chinese Academy of Medical Sciences, Beijing.
Zhonghua Yi Xue Za Zhi. 1996 Mar;76(3):187-90.
To develop a new way to prevent vascular anastomotic sites from intimal hyperplasia, we applied medical suture which had been soaked in pN2-pro-uk plasmid solution to perform rat carotid artery end-to-end anastomosis and study the effect of gene therapy with pro-uk gene on the formation of intimal hyperplasia of vascular anastomotic sites.
11/0 nylon medical suture which had been soaked in pN2-pro-uk plasmid solution was applied to perform rat carotid artery end to end anastomoses. The rats were randomly divided into control and treatment groups. In the control group, medical suture was soaked in the pN2 plasmid solution for 72 hours before use. In the treatment group, medical suture was soaked in the pN2-pro-uk plasmid solution. By means of Northern blot analysis, pro-urokinase activity assay, the number detection of cr-51 labelled platelets accumulating at anastomotic sites, 3H-TDR incorporation detection of anastomotic sites, pathological changes study, the following results were obtained.
When isolated RNA was hybridized with the radiolabeled pro-uk probe, band appeared in Northern blot analysis in the treatment group, but band could not be found in the control group. The pro-uk activity could be detected on the 2nd, 7th, 14th, 90th day in the treatment group, but could not be detected in the control group. The number of platelets accumulating at the anastomotic sites, the average intimal area and 3H-TDR incorporation of anastomotic sites were significantly fewer in the treatment group than in the control group (P < 0.01).
When medical suture which has been soaked in pN2-pro-uk plasmid solution is used to perform vascular anastomoses, the foreign gene can produce pro-uk at anastomotic sites and effectively prevent the formation of intimal hyperplasia. The mechanism is probably related to the decrease of platelets accumulating at anastomotic sites. This study provides a new way to prevent vascular anastomotic sites from intimal hyperplasia.
为开发一种预防血管吻合口内膜增生的新方法，我们应用浸泡于pN2-pro-uk质粒溶液中的医用缝线进行大鼠颈动脉端端吻合，并研究pro-uk基因治疗对血管吻合口内膜增生形成的影响。
应用浸泡于pN2-pro-uk质粒溶液中的11/0尼龙医用缝线进行大鼠颈动脉端端吻合。将大鼠随机分为对照组和治疗组。对照组在使用前将医用缝线浸泡于pN2质粒溶液中72小时。治疗组将医用缝线浸泡于pN2-pro-uk质粒溶液中。通过Northern印迹分析、尿激酶原活性测定、吻合口处铬-51标记血小板聚集数量检测、吻合口处3H-TDR掺入检测、病理变化研究，获得以下结果。
当分离的RNA与放射性标记的pro-uk探针杂交时，治疗组在Northern印迹分析中出现条带，而对照组未发现条带。治疗组在第2、7、14、90天可检测到尿激酶原活性，而对照组未检测到。治疗组吻合口处血小板聚集数量、平均内膜面积和吻合口处3H-TDR掺入均显著少于对照组（P<0.01）。
当使用浸泡于pN2-pro-uk质粒溶液中的医用缝线进行血管吻合时，外源基因可在吻合口处产生尿激酶原，有效预防内膜增生的形成。其机制可能与吻合口处血小板聚集减少有关。本研究为预防血管吻合口内膜增生提供了一种新方法。
