Myricitrin Delays Caenorhabditis elegans Aging: Association with DAF-16, SIR-2.1, and Potential Cholinergic Modulation.
- 1School of Life Sciences, Sichuan Normal University, Chengdu 610101, China.
Abstract
Background
Aging involves progressive functional decline driven by oxidative stress and mitochondrial dysfunction, and dietary flavonoids are promising aging interventions due to their multi-target regulatory pathways.Methods
This study systematically evaluated the anti-aging activity of myricitrin (MYR) and its underlying mechanisms using Caenorhabditis elegans, testing MYR at 0.25 mg/mL, employing a rotenone-induced model of mitochondrial oxidative stress, and performing reporter strain analyses, qRT-PCR, and molecular docking analysis with acetylcholinesterases (ACE-1/2).Results
MYR at 0.25 mg/mL significantly extended lifespan and improved locomotor performance without detectable toxicity regarding growth, feeding, or reproduction; reduced reactive oxygen species accumulation and restored antioxidant enzyme activities in the rotenone-induced model; was accompanied by the nuclear translocation of DAF-16 and the upregulation of associated downstream antioxidant genes (sod-3, gst-4); enhanced mitochondrial quality control by upregulating sir-2.1 and modulating genes associated with the mitochondrial unfolded protein response (atfs-1, hsp-6) and mitochondrial dynamics (fzo-1, drp-1); and indicated a favorable interaction between MYR and acetylcholinesterases (ACE-1/2).Conclusions
MYR represents a promising candidate compound for mitigating aging-related phenotypes, with its beneficial effects linked to a DAF-16-associated antioxidant response and SIR-2.1-correlated mitochondrial quality control network.
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BibTeX
@article{yang2026myricitrin,
title = {{Myricitrin Delays Caenorhabditis elegans Aging: Association with DAF-16, SIR-2.1, and Potential Cholinergic Modulation.}},
author = {Lijun Yang and Jiuyi Li and Yihan Zhou and Huaying Xu and Yu Wang and Jiayuan Zhao and Yanan Wang},
journal = {Antioxidants (Basel, Switzerland)},
year = {2026},
month = sep,
doi = {10.3390/antiox15101230},
url = {https://europepmc.org/article/MED/42939805},
note = {CC BY},
}
RIS
TY - JOUR
TI - Myricitrin Delays Caenorhabditis elegans Aging: Association with DAF-16, SIR-2.1, and Potential Cholinergic Modulation.
AU - Lijun Yang
AU - Jiuyi Li
AU - Yihan Zhou
AU - Huaying Xu
AU - Yu Wang
AU - Jiayuan Zhao
AU - Yanan Wang
PY - 2026
DA - 2026/09/23
JO - Antioxidants (Basel, Switzerland)
DO - 10.3390/antiox15101230
UR - https://europepmc.org/article/MED/42939805
AB - Background Aging involves progressive functional decline driven by oxidative stress and mitochondrial dysfunction, and dietary flavonoids are promising aging interventions due to their multi-target regulatory pathways.Methods This study systematically evaluated the anti-aging activity of myricitrin (MYR) and its underlying mechanisms using Caenorhabditis elegans, testing MYR at 0.25 mg/mL, employing a rotenone-induced model of mitochondrial oxidative stress, and performing reporter strain analyses, qRT-PCR, and molecular docking analysis with acetylcholinesterases (ACE-1/2).Results MYR at 0.25 mg/mL significantly extended lifespan and improved locomotor performance without detectable toxicity regarding growth, feeding, or reproduction; reduced reactive oxygen species accumulation and restored antioxidant enzyme activities in the rotenone-induced model; was accompanied by the nuclear translocation of DAF-16 and the upregulation of associated downstream antioxidant genes (sod-3, gst-4); enhanced mitochondrial quality control by upregulating sir-2.1 and modulating genes associated with the mitochondrial unfolded protein response (atfs-1, hsp-6) and mitochondrial dynamics (fzo-1, drp-1); and indicated a favorable interaction between MYR and acetylcholinesterases (ACE-1/2).Conclusions MYR represents a promising candidate compound for mitigating aging-related phenotypes, with its beneficial effects linked to a DAF-16-associated antioxidant response and SIR-2.1-correlated mitochondrial quality control network.
SN - 2076-3921
ER -