摘要
大量证据表明,一个增强的氧化和硝化应激可能在神经退行性疾病如阿尔茨海默病的发病机制中发挥核心作用。n-3多不饱和脂肪酸(n-3 PUFA)对氧化/硝化应激性损伤神经组织的抑制作用最近收到越来越多的关注。许多人实验研究来一致论证它们可以发挥实质性的预防作用,尤其是在阿尔茨海默病前的轻度认知障碍(MCI)的早期阶段。它已经表明,他们可以通过间接参与神经组织的氧化应激调制的几种蛋白质的表达/活动产生间接的抗氧化/反硝化作用。特别是最近的数据支持了假设在早期阶段的轻度认知障碍轻度到中度的氧化应激引发的细胞毒性剂n - 3多不饱和脂肪酸可以积极调节的转录活动核因子红细胞两个相关因子2(Nrf2)。这可能会导致血红素加氧酶-1(HO-1)的诱导表达及其他抗氧化蛋白Nrf2转录调节。另外,抗炎和抗氧化/反硝化作用的n-3多不饱和脂肪酸已发现和在参与神经退行性疾病的发病过程中他们冲小胶质细胞持续激活慢性炎症发生的能力相关。证据已经提交,n-3多不饱和脂肪酸可将小胶质细胞的巨噬细胞M1到M2表型显示低生产氧化活性神经毒性因素和增强吞噬细胞的对Aβ多肽吞噬力,甚至是神经营养/保护性的进一步表型。
关键词: 阿尔茨海默病,抗氧化,HO-1,小胶质细胞,Nrf2,n-3多不饱和脂肪酸
Current Alzheimer Research
Title:Reduction of Oxidative/Nitrosative Stress in Brain and its Involvement in the Neuroprotective Effect of n-3 PUFA in Alzheimer’s Disease
Volume: 13 Issue: 2
Author(s): Simona Serini and Gabriella Calviello
Affiliation:
关键词: 阿尔茨海默病,抗氧化,HO-1,小胶质细胞,Nrf2,n-3多不饱和脂肪酸
摘要: Plenty of evidence has shown that an enhanced oxidative or nitrosative stress may play a central role in the pathogenesis of neurodegenerative disorders such as Alzheimer’s disease (AD). The suppressive effect of n-3 polyunsaturated fatty acids (n-3 PUFA) against oxidative/nitrosative stressinduced injury in nervous tissues has recently received increasing interest. A number of human experimental studies have concurred to demonstrate that they may exert a substantial preventive role, especially in the very early phase of mild cognitive impairment (MCI) preceding AD. It has been suggested that they may exert an indirect antioxidant/anti-nitrosative role by modulating the expression/ activity of several proteins involved in the modulation of oxidative stress in nervous tissues. In particular, recent data have supported the hypothesis that in the early phase of MCI the light to moderate oxidative stress triggered by not cytotoxic doses of n-3 PUFA can positively regulate the transcriptional activity of nuclear factor erythroid 2-related factor 2 (Nrf2). This may result in the induced expression of heme oxygenase-1 (HO-1) and other antioxidant proteins transcriptionally regulated by Nrf2. Alternatively, the anti-inflammatory and antioxidant/anti-nitrosative effects of n-3 PUFA have been lately related to their ability to blunt microglia persistent activation occurring during chronic inflammation involved in the pathogenesis of neurodegenerative diseases. Evidences have been presented that n-3 PUFA may convert microglia from the macrophage M1 to an M2 phenotype showing lower production of neurotoxicoxidative factors and enhanced phagocytic activity toward Aβ peptide, or even to a further phenotype with neurotrophic/ protective properties.
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Simona Serini and Gabriella Calviello , Reduction of Oxidative/Nitrosative Stress in Brain and its Involvement in the Neuroprotective Effect of n-3 PUFA in Alzheimer’s Disease, Current Alzheimer Research 2016; 13 (2) . https://dx.doi.org/10.2174/1567205012666150921101147
DOI https://dx.doi.org/10.2174/1567205012666150921101147 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
Call for Papers in Thematic Issues
Current updates on the Role of Neuroinflammation in Neurodegenerative Disorders
Neuroinflammation is an invariable hallmark of chronic and acute neurodegenerative disorders and has long been considered a potential drug target for Alzheimer?s disease (AD) and dementia. Significant evidence of inflammatory processes as a feature of AD is provided by the presence of inflammatory markers in plasma, CSF and postmortem brain ...read more
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