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Updated: Oct 28, 2026
Using Caenorhabditis elegans as a Model System to Study Protein Homeostasis in a Multicellular Organism
Published on: December 18, 2013
Myricitrin Delays Caenorhabditis elegans Aging: Association with DAF-16, SIR-2.1, and Potential Cholinergic
Lijun Yang1, Jiuyi Li1, Yihan Zhou1
1School of Life Sciences, Sichuan Normal University, Chengdu 610101, China.
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.
