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类胡萝卜素通过 Ins/IGF-1 信号对细胞的补充保护作用延长了秀丽隐杆线虫的寿命。

Supplemental cellular protection by a carotenoid extends lifespan via Ins/IGF-1 signaling in Caenorhabditis elegans.

机构信息

Department of Health Science, Daito Bunka University School of Sports and Health Science, Iwadono 560, Higashi-matsuyama, Saitama 355-8501, Japan.

出版信息

Oxid Med Cell Longev. 2011;2011:596240. doi: 10.1155/2011/596240. Epub 2011 Oct 12.

DOI:10.1155/2011/596240
PMID:22013497
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3195502/
Abstract

Astaxanthin (AX), which is produced by some marine animals, is a type of carotenoid that has antioxidative properties. In this study, we initially examined the effects of AX on the aging of a model organism C. elegans that has the conserved intracellular pathways related to mammalian longevity. The continuous treatments with AX (0.1 to 1 mM) from both the prereproductive and young adult stages extended the mean lifespans by about 16-30% in the wild-type and long-lived mutant age-1 of C. elegans. In contrast, the AX-dependent lifespan extension was not observed even in a daf-16 null mutant. Especially, the expression of genes encoding superoxide dismutases and catalases increased in two weeks after hatching, and the DAF-16 protein was translocated to the nucleus in the AX-exposed wild type. These results suggest that AX protects the cell organelle mitochondria and nucleus of the nematode, resulting in a lifespan extension via an Ins/IGF-1 signaling pathway during normal aging, at least in part.

摘要

虾青素(AX)是某些海洋动物产生的一种类胡萝卜素,具有抗氧化特性。在这项研究中,我们首先研究了 AX 对具有与哺乳动物长寿相关的保守细胞内途径的模式生物秀丽隐杆线虫衰老的影响。从生殖前和幼年期开始,用 AX(0.1 至 1mM)连续处理可使野生型和长寿突变体 age-1 的秀丽隐杆线虫的平均寿命延长约 16-30%。相比之下,即使在 daf-16 缺失突变体中也观察不到 AX 依赖性的寿命延长。特别是,在孵化后两周内,编码超氧化物歧化酶和过氧化氢酶的基因表达增加,并且在暴露于 AX 的野生型中 DAF-16 蛋白被转位到细胞核中。这些结果表明,AX 保护线虫的细胞器线粒体和细胞核,至少部分通过正常衰老过程中的 Ins/IGF-1 信号通路延长寿命。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87f2/3195502/6ec4f77b4773/OXIMED2011-596240.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87f2/3195502/328d17f8e1d2/OXIMED2011-596240.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87f2/3195502/8d7f6d4598c1/OXIMED2011-596240.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87f2/3195502/aebff1b2806f/OXIMED2011-596240.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87f2/3195502/d36aa8c359ca/OXIMED2011-596240.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87f2/3195502/6ec4f77b4773/OXIMED2011-596240.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87f2/3195502/328d17f8e1d2/OXIMED2011-596240.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87f2/3195502/8d7f6d4598c1/OXIMED2011-596240.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87f2/3195502/aebff1b2806f/OXIMED2011-596240.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87f2/3195502/d36aa8c359ca/OXIMED2011-596240.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87f2/3195502/6ec4f77b4773/OXIMED2011-596240.005.jpg

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