MITOCHONDRIAL TARGETED ANTIOXIDANT THERAPEUTICS IN MULTIPLE SCLEROSIS

多发性硬化症的线粒体靶向抗氧化治疗

• 批准号: 8173322
• 负责人: P. Hemachandra Reddy
• 金额: $ 5.71万
• 依托单位: OREGON HEALTH & SCIENCE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-05-01 至 2011-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8173322
• 关键词: Activities of Daily Living; Animal Model; Antioxidants; Cell Culture System; Chronic; Computer Retrieval of Information on Scientific Projects Database; Demyelinations; Disease; Economics; Experimental Autoimmune Encephalomyelitis; Funding; Grant; Healthcare; In Vitro; Institution; Mediator of activation protein; Mitochondria; Multiple Sclerosis; Oxidative Stress; Pathogenesis; Play; Property; Reactive Oxygen Species; Research; Research Personnel; Resources; Role; Social Impacts; Source; Therapeutic; United States National Institutes of Health; cost; disability; in vivo; macrophage; multidisciplinary; neuroprotection; productivity loss; social; young adult

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Multiple Sclerosis (MS) is a chronic and potentially highly disabling disorder with considerable social impact and economic consequences. It is the major cause of non-traumatic disability in young adults. The social costs associated with MS are high because of its long duration, the early loss of productivity, the need for assistance in activities of daily living and the use of immunomodulatory treatments and multidisciplinary health care. Increasing evidence suggests that oxidative stress plays a major role in the pathogenesis of MS. Reactive oxygen species (ROS), leading to oxidative stress, generated in excess primarily by macrophages, have been implicated as mediators of demyelination and axonal damage in both MS and experimental autoimmune encephalomyelitis (EAE), its animal model. Recently, we found that the mitochondrial targeted antioxidant, MitoQ has a neuroprotection role through its antioxidative property. We hypothesize that MitoQ may have a protection or curative role in MS, thus we will use cell culture system (in vitro) and animal model (in vivo) to examine this new idea. This proposal may open a new window for treatment of MS.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目及 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 多发性硬化症 (MS) 是一种慢性且可能高度致残的疾病，具有相当大的社会影响和经济后果。它是年轻人非创伤性残疾的主要原因。与多发性硬化症相关的社会成本很高，因为其病程长、生产力较早丧失、日常生活活动需要协助以及免疫调节治疗和多学科医疗保健的使用。越来越多的证据表明，氧化应激在多发性硬化症的发病机制中起着重要作用。活性氧（ROS）会导致氧化应激，主要由巨噬细胞过量产生，在多发性硬化症及其动物模型实验性自身免疫性脑脊髓炎（EAE）中被认为是脱髓鞘和轴突损伤的介质。最近，我们发现线粒体靶向抗氧化剂 MitoQ 通过其抗氧化特性具有神经保护作用。我们假设MitoQ可能对MS有保护或治疗作用，因此我们将使用细胞培养系统（体外）和动物模型（体内）来检验这个新想法。该提议可能为多发性硬化症的治疗打开一个新的窗口。