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磷脂酰胆碱通过 DAF-16 延长寿命并降低. 中的淀粉样β诱导的毒性。

Phosphatidylcholine Extends Lifespan via DAF-16 and Reduces Amyloid-Beta-Induced Toxicity in .

机构信息

Department of Medical Biotechnology, Soonchunhyang University, Asan 31538, Republic of Korea.

出版信息

Oxid Med Cell Longev. 2019 Jul 11;2019:2860642. doi: 10.1155/2019/2860642. eCollection 2019.

DOI:10.1155/2019/2860642
PMID:31379987
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6657616/
Abstract

Phosphatidylcholine is one of the major phospholipids comprising cellular membrane and is known to have several health-promoting activities, including the improvement of brain function and liver repair. In this paper, we examine the effect of dietary supplementation with phosphatidylcholine on the response to environmental stressors and aging in . Treatment with phosphatidylcholine significantly increased the survival of worms under oxidative stress conditions. However, there was no significant difference in response to stresses caused by heat shock or ultraviolet irradiation. Oxidative stress is believed to be one of the major causal factors of aging. Then, we examined the effect of phosphatidylcholine on lifespan and age-related physiological changes. Phosphatidylcholine showed a lifespan-extending effect and a reduction in fertility, possibly as a tradeoff for long lifespan. Age-related decline of motility was also significantly delayed by supplementation with phosphatidylcholine. Interestingly, the expressions of well-known longevity-assuring genes, and , were significantly upregulated by dietary intervention with phosphatidylcholine. DAF-16, a transcription factor modulating stress response genes, was accumulated in the nucleus by phosphatidylcholine treatment. Increase of the ROS level with phosphatidylcholine suggests that the antioxidant and lifespan-extending effects are due to the hormetic effect of phosphatidylcholine. Phosphatidylcholine also showed a protective effect against amyloid beta-induced toxicity in Alzheimer's disease model animals. Experiments with long-lived mutants revealed that the lifespan-extending effect of phosphatidylcholine specifically overlapped with that of reduced insulin/IGF-1-like signaling and required DAF-16. These findings showed the antioxidant and antiaging activities of phosphatidylcholine for the first time . Further studies focusing on the identification of underlying cellular mechanisms involved in the antiaging effect will increase the possibility of using phosphatidylcholine for the development of antiaging therapeutics.

摘要

磷脂酰胆碱是构成细胞膜的主要磷脂之一,已知具有多种促进健康的作用,包括改善大脑功能和肝脏修复。在本文中,我们研究了饮食补充磷脂酰胆碱对环境应激和衰老的影响。用磷脂酰胆碱处理可显著提高线虫在氧化应激条件下的存活率。然而,对热休克或紫外线照射引起的应激的反应没有显著差异。氧化应激被认为是衰老的主要原因之一。然后,我们研究了磷脂酰胆碱对寿命和与年龄相关的生理变化的影响。磷脂酰胆碱表现出延长寿命和降低生育能力的作用,这可能是为了换取长寿命。补充磷脂酰胆碱还显著延缓了运动能力随年龄的下降。有趣的是,已知的保证长寿的基因和的表达,通过饮食干预磷脂酰胆碱显著上调。DAF-16,一种调节应激反应基因的转录因子,被磷脂酰胆碱处理积累在核内。磷脂酰胆碱增加 ROS 水平表明,其抗氧化和延长寿命的作用是由于磷脂酰胆碱的有益效应。磷脂酰胆碱在阿尔茨海默病模型动物中也显示出对淀粉样β诱导的毒性的保护作用。对长寿突变体的实验表明,磷脂酰胆碱的延长寿命作用与胰岛素/IGF-1样信号的降低特异性重叠,并需要 DAF-16。这些发现首次表明了磷脂酰胆碱的抗氧化和抗衰老活性。进一步研究集中在鉴定与抗衰老作用相关的细胞机制,将增加使用磷脂酰胆碱开发抗衰老治疗的可能性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30f0/6657616/a2dfc6d3bf8a/OMCL2019-2860642.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30f0/6657616/a3d5cc20a4d9/OMCL2019-2860642.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30f0/6657616/b87555a7143d/OMCL2019-2860642.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30f0/6657616/ba5bc9281e96/OMCL2019-2860642.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30f0/6657616/9c3ae49ed63e/OMCL2019-2860642.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30f0/6657616/9a0a4a304ed7/OMCL2019-2860642.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30f0/6657616/c57607c4302c/OMCL2019-2860642.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30f0/6657616/a2dfc6d3bf8a/OMCL2019-2860642.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30f0/6657616/a3d5cc20a4d9/OMCL2019-2860642.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30f0/6657616/b87555a7143d/OMCL2019-2860642.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30f0/6657616/ba5bc9281e96/OMCL2019-2860642.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30f0/6657616/9c3ae49ed63e/OMCL2019-2860642.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30f0/6657616/9a0a4a304ed7/OMCL2019-2860642.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30f0/6657616/c57607c4302c/OMCL2019-2860642.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30f0/6657616/a2dfc6d3bf8a/OMCL2019-2860642.007.jpg

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