Ellagic Acid Increases Stress Resistance via Insulin/IGF-1 Signaling Pathway in <i>Caenorhabditis elegans</i>

Ellagic acid is a natural polyphenol found in various fruits and vegetables. Numerous studies have shown that ellagic acid has beneficial effects on human health. In this study, we investigated the stress resistant action of ellagic acid in <i>Caenorhabditis elegans</i> (<i>C. eleg...

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Bibliographic Details
Published in:Molecules
Main Authors: Shuju Bai, Yaoru Yu, Lu An, Wenbo Wang, Xueqi Fu, Jing Chen, Junfeng Ma
Format: Article
Language:English
Published: MDPI AG 2022-09-01
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Online Access:https://www.mdpi.com/1420-3049/27/19/6168
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Summary:Ellagic acid is a natural polyphenol found in various fruits and vegetables. Numerous studies have shown that ellagic acid has beneficial effects on human health. In this study, we investigated the stress resistant action of ellagic acid in <i>Caenorhabditis elegans</i> (<i>C. elegans</i>). Notably, 50 μM ellagic acid prolonged the lifespan of <i>C. elegans</i> by 36.25%, 36.22%, 155.1%, and 79.07% under ultraviolet radiation stress, heat stress, oxidative stress, and <i>Pseudomonas aeruginosa</i> infection stress, respectively. Furthermore, the mechanism by which ellagic acid reduces the damage caused by ultraviolet radiation in <i>C. elegans</i> was explored. Ellagic acid could significantly induce the nucleus translocation of DAF-16 and, thereby, activate a series of target genes to resist ultraviolet radiation stress. Moreover, ellagic acid also significantly increased the expression of SOD-3 by 3.61 times and the activity of superoxide dismutase by 3.70 times to clean out harmful reactive oxygen species in <i>C. elegans</i> exposed to ultraviolet radiation stress. In both <i>daf-16</i> mutant and <i>daf-2</i>; <i>daf-16</i> double-mutant worms exposed to ultraviolet radiation, ellagic acid could no longer prolong their lifespan. These results indicate that ellagic acid plays an important role in resisting ultraviolet radiation stress in <i>C. elegans,</i> probably in an insulin/IGF-1 signaling pathway-dependent way.
ISSN:1420-3049