Reduction of Cerebral Oxidative Stress Following Environmental Enrichment in Mice with Alzheimer-Like Pathology
Reduction of Cerebral Oxidative Stress Following Environmental Enrichment in Mice with Alzheimer-Like Pathology
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DOI：
10.1111/j.1750-3639.2008.00257.x
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发表时间：
2010-01-01
期刊：
影响因子：
6.4
通讯作者：
Keyvani, Kathy
中科院分区：
文献类型：
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作者：
Herring, Arne;Blome, Mareike;Keyvani, Kathy
氧化应激是慢性神经退行性疾病（如阿尔茨海默病）进展过程中的一个关键特征。在衰老的人类和动物中，自愿运动可以降低氧化应激反应。此外，我们实验室最近的工作表明，认知和物理刺激（称为环境富集）抵消了阿尔茨海默病样小鼠的淀粉样蛋白β病理，神经血管功能障碍和行为症状。基于这些事实，我们假设认知和身体活动也可以保护阿尔茨海默病大脑免受氧化应激。因此，我们将雌性TgCRND 8小鼠从第30天至5月龄保持在标准和富集的饲养条件下。环境刺激减弱了促氧化过程并触发了抗氧化防御机制，如活性氧和氮物质的生物标志物减少、促炎和促氧化介质下调、促凋亡半胱天冬酶表达减少以及SOD 1和SOD 2上调所示。这项研究确定了一个迄今为止尚未描述的拮抗作用的环境刺激对阿尔茨海默氏病相关的氧化损伤。
Oxidative stress is a key feature during progression of chronic neurodegenerative conditions such as Alzheimer's disease. In aging humans and animals, voluntary exercise lowers oxidative stress reactions. Additionally, recent work in our lab demonstrated that cognitive and physical stimulation (termed environmental enrichment) counteracts amyloid beta pathology, neurovascular dysfunction and behavioral symptoms in mice with Alzheimer-like disease. Based on these facts, we hypothesized that cognitive and physical activity can also protect against oxidative stress in Alzheimer-diseased brain. We, therefore, kept female TgCRND8 mice under standard and enriched housing from day 30 until 5 months of age. Environmental stimulation attenuated pro-oxidative processes and triggered anti-oxidative defense mechanisms as indicated by diminished biomarkers for reactive oxygen and nitrogen species, downregulation of pro-inflammatory and pro-oxidative mediators, decreased expression of pro-apoptotic caspases, and upregulation of SOD1 and SOD2. This study identifies a thus far undescribed antagonizing effect of environmental stimulation on Alzheimer's disease-related oxidative damage.