神经保护
炎症
一氧化氮
背景(考古学)
中枢神经系统
医学
神经科学
缺血
调解人
免疫系统
免疫学
药理学
心理学
生物
内科学
古生物学
作者
Marisol Godínez‐Rubí,Daniel Ortuño‐Sahagún
出处
期刊:Elsevier eBooks
[Elsevier]
日期:2017-01-01
卷期号:: 263-292
标识
DOI:10.1016/b978-0-12-809275-0.00011-9
摘要
The central nervous system (CNS) is able to raise an immune response against the majority of threatening stimuli, but the control of early CNS inflammation is critical, because too much or too little inflammation will lead to a decrease or a delay in recovery. Whether the inflammation is neurotoxic or protective may depend upon the context and the location of the inflammatory mediator in relation to an injury or an affliction, and also depends on the timing of the inflammatory response, which may determine its outcome. Nitric oxide (NO) is a signaling molecule that participates in numerous physiological processes, including regulation of vascular tone, neurotransmission, and immunomodulation. Here, we review NO participation in three different etiologies for brain damage: traumatic brain injury, ischemia–reperfusion damage, and Alzheimer's disease. We focus on the dual action of NO as a neurotoxic or neuroprotective agent, which mainly depends on its concentration, compartmentation (localization), source, environment, and the enzyme and cells producing it. Finally, we present a comprehensive review of evidences that argue about the use of NO donors as adjuvant neuroprotective agents in different therapies for brain inflammation.
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