Journal of Functional Foods· 2026Q1
Theaflavin monomers extend Caenorhabditis elegans lifespan through insulin/IGF-1 signaling pathway
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- Q1SCImago
- 2026year
Short summary
Theaflavin monomers TF1 (100 μM) and TF2B (500 μM) extended lifespan in C. elegans by suppressing the DAF-2 insulin/IGF-1 signaling pathway, dependent on DAF-16/FOXO.
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Key points
- Theaflavin monomers TF1 (100 μM) and TF2B (500 μM) significantly increased C. elegans lifespan.
- These monomers suppressed the DAF-2-mediated insulin/IGF-1 signaling pathway.
- Lifespan extension was dependent on the DAF-16/FOXO transcription factor.
- TF1 upregulated genes related to the ubiquitin-proteasome system.
AI-generated from the title and abstract; the full text is not read.
Abstract
Aging is a vital contributor to numerous disorders, including diabetes, cardiovascular illnesses, and neurodegeneration. Theaflavins (TFs) exert anti-aging effects, including antioxidant, anti-inflammatory, and neuroprotective activities. Nevertheless, prior investigations mainly employed crude TF extracts, while the anti-aging active monomers and their molecular mechanisms remain unclear. This study investigated the anti-aging activities of the main monomeric compounds of TFs in Caenorhabditis elegans and explored the molecular mechanism. 100 μM TF1 and 500 μM TF2B markedly increased lifespan, enhanced resistance, and reduced lipofuscin accumulation without affecting reproductive capacity. Mechanistically, TF1 and TF2B suppressed the DAF-2-mediated insulin/IGF-1 signaling pathway. The lifespan-extending effect relied on the DAF-16/FOXO transcription factor and was independent of dietary restriction, as supported by molecular docking and mutant strain validation. Furthermore, TF1 upregulated the ubiquitin-proteasome system-related gene levels. This research revealed the molecular mechanisms for the anti-aging activity of theaflavin monomers and supports tea-based dietary strategies for healthy aging.
The authors' abstract, as published at the source. Journal of Functional Foods, 2026 · DOI ↗
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AgingBiochemistry, Genetics and Molecular Biology