FREE RADICALS, APOPTOSIS & TREATMENT OF DECUBITUS ULCERS
FREE RADICALS, APOPTOSIS & TREATMENT OF DECUBITUS ULCERS
批准号:
2203933
负责人:
RICHARD SALCIDO
金额:
$15.07万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
1994
资助国家:
美国
项目状态:
已结题
起止时间:
1994-01-01 至 1996-12-31
关键词:
aging animal age group animal old age antioxidants apoptosis decubitus ulcer disease /disorder model electron spin resonance spectroscopy enzyme activity free radical oxygen glutamate ammonia ligase histopathology hydroxyl radical ischemia juvenile animal laboratory rat mechanical pressure reperfusion salicylate ultrasound blood flow measurement
中文摘要
这项研究是康复部门共同努力的结果
医学、药理学和生物医学工程中心。
尽管压疮(PS)的发病率和成本很高,但几乎没有
科学研究已转向生物化学和分子生物学
溃疡形成的机制,从而阻碍有效的治疗。
PS的临床研究很难评估,因为它们经常
定性的、经验的和不受控制的。我们的电脑控制的动物
模型允许对建议的
PS治疗和预防。这个系统使我们能够调查
脑缺血再灌注损伤与自由基的关系
(FR)通过将生化事件与非侵入性联系起来进行生产
使用激光多普勒血流计测量血流量。压力
溃疡被认为是由于对潜在疾病的IR/侮辱而形成的
皮下组织(肌肉和/或脂肪组织)。目前的提案
旨在直接确定
压力/缺血持续时间和频率与心肌梗死的最终发展
PS.对自由基(FR)产生的测量将验证
FR参与PS发生的病理生理学过程。FR自旋-
将对诱捕化合物和其他试剂的能力进行评估
限制或阻止PS的发展。我们对分子的研究
PS的原因将继续随着我们的假设的检验而继续
细胞凋亡(程序性细胞死亡)可能在
压疮的形成。FR、细胞凋亡和PS关系密切
与细胞死亡有关。如果发现了细胞凋亡,有几种治疗方法
会有牵连(即使用蛋白质和/或RNA的抑制剂
综合)。
英文摘要
This study is a joint effort of the departments of Rehabilitation
Medicine, Pharmacology, and the Center for Biomedical Engineering.
Despite the high prevalence and cost of pressure sores (PS), little
scientific study has been directed towards the biochemical and molecular
mechanisms of ulcer development, thus hampering effective treatment.
Clinical studies on PS are difficult to assess because they are often
qualitative, empirical, and uncontrolled. Our computer-controlled animal
model allows for rigorous scientific analysis and evaluation of proposed
PS treatments and preventatives. This system allows us to investigate the
relationship between ischemia/reperfusion (IR) injury and free radical
(FR) production by relating the biochemical events to the noninvasive
measurement of blood flow utilizing a laser Doppler flow meter. Pressure
ulcers are thought to develop as a result of IR/insult of the underlying
subcutaneous tissue (muscle and/or adipose tissue). The current proposal
is designed to directly determine the relationship between
pressure/ischemia duration and frequency and the ultimate development of
PS. Measurement of free radical (FR) production will verify the
involvement of FR in the pathophysiology of PS development. FR spin-
trapping compounds and other agents will be evaluated as to their ability
to limit or prevent the development of PS. Our investigation of molecular
causes of PS will continue with the testing of our hypothesis that
apoptosis (programmed cell death) may play a significant role in the
formation of decubitus ulcers. FR, apoptosis, and PS are intimately
associated with cell death. If apoptosis is identified, several treatments
would be implicated (i.e. use of inhibitors of protein and/or RNA
synthesis).
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