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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.

该实验室的目标是确定肠道修复机制以利于受伤肠道的恢复。肠缺血再灌注损伤因其在马绞痛综合症，马的主要杀手。一个模型猪将会出现缺血/再灌注损伤。有可能猪将为人类和马提供更好的模型，因为黄嘌呤氧化酶水平相似。亲戚缺血和再灌注对肠道损伤的贡献决定。缺血性损伤似乎对大型动物更为重要物种比再灌注损伤，与啮齿动物模型相反，其中再灌注损伤较为突出。由于未能阻止再灌注马的受伤，以及啮齿动物模型的可疑相关性人体再灌注损伤后，其修复过程就会有特点。谷氨酰胺 (GLN) 和生长因子增强增殖的能力将研究 GLN 促进修复的机制他会检查。具体而言，Jun 核激酶的激活和丝裂原激活激酶，对于诱导“早期- 将评估直接”基因。这些研究应提供基本的有关上皮增殖和替代机制的信息缺血性损伤的治疗方法。