权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

MECHANISMS OF REPAIR OF ISCHEMIC INJURED INTESTINE

缺血性损伤肠的修复机制

基本信息

批准号：
2668278
负责人：
ANTHONY BLIKSLAGER
金额：
$ 3.6万
依托单位：
NORTH CAROLINA STATE UNIVERSITY RALEIGH
依托单位国家：
美国
项目类别：
财政年份：
1998
资助国家：
美国
起止时间：
1998-02-08 至
项目状态：
未结题

来源：
https://reporter.nih.gov/project-details/2668278
关键词：
cell cycle disease /disorder model gastrointestinal epithelium glutamine intestine disorder ischemia mitogen activated protein kinase oxidative stress reperfusion swine transforming growth factors xanthine dehydrogenase xanthine oxidase

项目摘要

The goal of this laboratory is to identify mechanisms of intestinal repair in order to facilitate recovery of injured intestine. Intestinal ischemial reperfusion injury is of particular interest because of its role in the equine colic syndrome, the principal killer of horses. A model of ischemia/ reperfusion injury will be developed in the pig. It is possible that the pig will provide a better model for the human and the horse, because of similar low levels of xanthine oxidase. The relative contribution of ischemia and reperfusion to intestinal injury will be determined. Ischemic injury appears to he more important in large animal species than reperfusion injury, as opposed to rodent models in which reperfusion injury is prominent. Because of a failure to block reperfusion injury in the horse, and the questionable relevance of rodent models of reperfusion injury to the human, the repair process will be characterized. The ability of glutamine (GLN) and growth factors to enhance proliferation will be investigated, and the mechanism by which GLN facilitates repair will he examined. Specifically, activation of Jun-nuclear kinase and Mitogen-activated kinase, enzymes critical for the induction of "early- immediate" genes, will be assessed. These studies should provide basic information on mechanisms of epithelial proliferation and alternative therapeutic approaches to ischemic injury.

这个实验室的目标是确定肠道修复的机制以促进受损肠的恢复。肠缺血再灌注损伤是特别感兴趣的，因为它在脑缺血中的作用。马绞痛综合症，马的主要杀手。的典范将在猪中产生缺血/再灌注损伤。可以猪将为人类和马提供一个更好的模型，因为黄嘌呤氧化酶的水平也很低。的相对缺血和再灌注对肠损伤的贡献将是测定缺血性损伤在大型动物中显得更为重要物种比再灌注损伤，而不是啮齿动物模型，其中再灌注损伤显著。由于未能阻断再灌注马的伤害，以及啮齿动物模型的可疑相关性，再灌注损伤的人，修复过程的特点。谷氨酰胺（GLN）和生长因子促进增殖的能力将被调查，GLN促进修复的机制他将检查。具体而言，Jun-nuclear kinase和丝裂原活化激酶，对诱导“早期- 将评估“立即”基因。这些研究提供了基本的关于上皮细胞增殖机制和替代方法的信息缺血性损伤的治疗方法。