What this means
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. 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).
A plain-English summary is on its way. Until then, this is the start of the authors' own summary.
- Who it was tested in
- Not stated
- Kind of research
- A study
The science
- Original title
- Myricitrin Delays Caenorhabditis elegans Aging: Association with DAF-16, SIR-2.1, and Potential Cholinergic Modulation.
- Authors
- Yang L, Li J, Zhou Y et al.
- Journal
- Antioxidants (Basel, Switzerland)
- Published
- Oct 27, 2026
- Study type
- Study
- PMID
- 42939805 ↗
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.
What they did
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).
What they found
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). 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.
The authors' abstract, grouped under plain headings from its own section labels.
Yang L, Li J, Zhou Y et al. Myricitrin Delays Caenorhabditis elegans Aging: Association with DAF-16, SIR-2.1, and Potential Cholinergic Modulation. Antioxidants (Basel, Switzerland). 2026. doi:10.3390/antiox15101230. PMID: 42939805. https://pubmed.ncbi.nlm.nih.gov/42939805/