• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Gene transfer of extracellular superoxide dismutase improves relaxation of aorta after treatment with endotoxin.
【24h】

Gene transfer of extracellular superoxide dismutase improves relaxation of aorta after treatment with endotoxin.

机译：细胞内超氧化物歧化酶的基因转移可改善内毒素治疗后的主动脉松弛。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Lipopolysaccharide (LPS) impairs vascular function, in part by generation of reactive oxygen species. One goal of this study was to determine whether gene transfer of extracellular SOD (ECSOD) improves vascular responsiveness in LPS-treated rats. A second goal was to determine whether effects of ECSOD are dependent on the heparin-binding domain of the enzyme, which facilitates binding of ECSOD to the outside of cells. Adenoviruses containing ECSOD (AdECSOD), ECSOD with deletion of its heparin-binding domain (AdECSOD-HBD), or a control virus (AdLacZ) were injected intravenously into rats. Three days later, vehicle or LPS (10 mg/kg ip) was injected. After 24 h, vascular reactivity was examined in aortic rings in vitro. Maximum relaxation to acetylcholine was 95 +/- 1% (means +/- SE) after AdlacZ plus vehicle and 77 +/- 3% after AdlacZ plus LPS (P < 0.05). Responses to calcium ionophore A-23187 and submaximal concentrations of nitroprusside also were impaired by LPS. Gene transfer of ECSOD, but not AdECSOD-HBD, improved (P < 0.05) relaxation to acetylcholine and A-23187 after LPS. Maximum relaxation to acetylcholine was 88 +/- 3% after LPS plus AdECSOD. Superoxide was increased in aorta after LPS, and the levels were reduced after AdECSOD but not AdECSOD-HBD. LPS-induced adhesion of leukocytes to aortic endothelium was reduced by AdECSOD but not by AdECSOD-HBD. We conclude that after gene transfer in vivo, binding of ECSOD to arteries effectively decreases the numbers of adherent leukocytes and levels of superoxide and improves impaired endothelium-dependent relaxation produced by LPS.
机译：脂多糖（LPS）部分地通过产生活性氧而损害血管功能。这项研究的目的之一是确定细胞外SOD（ECSOD）的基因转移是否能改善LPS治疗大鼠的血管反应性。第二个目标是确定ECSOD的作用是否取决于酶的肝素结合域，从而促进ECSOD与细胞外部的结合。将含有ECSOD（AdECSOD），具有肝素结合结构域缺失的ECSOD的腺病毒（AdECSOD-HBD）或对照病毒（AdLacZ）静脉内注射到大鼠中。三天后，注射媒介物或LPS（10 mg / kg ip）。 24小时后，体外检查主动脉环中的血管反应性。在加入AdlacZ和赋形剂后，对乙酰胆碱的最大弛豫为95 +/- 1％（平均+/- SE），在加入AdlacZ和LPS后达到77 +/- 3％（P <0.05）。 LPS也削弱了对钙离子载体A-23187的反应和亚硝普钠的最大浓度。 LPS后，ECSOD的基因转移而非AdECSOD-HBD的基因转移改善了对乙酰胆碱和A-23187的松弛（P <0.05）。 LPS加AdECSOD后，乙酰胆碱的最大舒张率为88 +/- 3％。 LPS后主动脉中的超氧化物增加，而AdECSOD后的水平降低，但AdECSOD-HBD的水平降低。 LPS诱导的白细胞与主动脉内皮细胞的粘附可通过AdECSOD降低，但不能通过AdECSOD-HBD降低。我们得出的结论是，在体内基因转移后，ECSOD与动脉的结合有效地减少了粘附白细胞的数量和超氧化物水平，并改善了LPS产生的内皮依赖性舒张功能受损。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号