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Nutrition foundations
Research brief

Perilla leaf extract extends lifespan and lowers fat in C. elegans worms

In the nematode C. elegans, an ethyl acetate extract of Perilla frutescens leaves lengthened lifespan, reduced lipid storage and oxidative markers, and activated the insulin/IGF-1 signaling pathway with DAF-16/FOXO and SKN-1/Nrf2. These are worm and biomarker results, not demonstrated human lifespan benefits. [1]

Automatic summary · not editorially reviewed

The key findings

  1. The study used the nematode Caenorhabditis elegans as model organism and tested an ethyl acetate extract of Perilla frutescens leaves (EAEPF). [1]

  2. EAEPF treatment significantly prolonged lifespan and markedly reduced lipid storage in the nematodes. [1]

  3. EAEPF activated the insulin/IGF-1 signaling pathway and upregulated DAF-16/FOXO and SKN-1/Nrf2, promoting stress-response genes. [1]

The source at a glance

Study type / format
Preclinical study in a nematode model (abstract)
Population / context
Caenorhabditis elegans nematode worms
Summary based on
Study abstract
Original publication
September 26, 2026

Perilla extract tested in C. elegans worms

The abstract describes a study using Caenorhabditis elegans, a nematode worm, as the model organism. The researchers tested an ethyl acetate extract of Perilla frutescens leaves, called EAEPF. Perilla is described as rich in flavonoids and other secondary metabolites with antioxidant properties. The stated aim was to explore lifespan-modulating effects and underlying mechanisms of this extract. No human participants were involved, and the abstract does not report a comparison group, sample sizes or follow-up periods.

Supporting source [1]

Longer worm lifespan and less lipid storage

According to the abstract, EAEPF treatment significantly prolonged lifespan in the worms. It also enhanced pharyngeal pumping and head thrashing frequencies, two measures of worm movement and function. The extract reduced accumulation of lipofuscin and reactive oxygen species, improved antioxidant enzyme activity, lowered malondialdehyde levels and increased resistance to thermal and juglone-induced oxidative stress. EAEPF markedly reduced lipid storage in the nematodes, which the authors describe as a lipid-lowering effect. These outcomes were measured in worms, so they do not establish effects on human health or aging.

Supporting source [1]

Insulin/IGF-1 pathway and proposed nutraceutical use

Mechanistically, the abstract states that EAEPF activated the insulin/IGF-1 signaling pathway and upregulated the transcription factors DAF-16/FOXO and SKN-1/Nrf2. These in turn promoted expression of downstream stress-response genes sod-3, gst-4 and hsp-16.2. EAEPF also reprogrammed lipid metabolism and enhanced glutathione metabolism. The authors suggest the extract may be a potential source of nutritional hormetins and a potential nutraceutical for lifespan extension and healthspan improvement. These are proposals based on worm data; the abstract does not show that such benefits occur in humans.

Supporting source [1]

How to interpret this

This is an abstract only; the full text was not reviewed. The work was done in C. elegans worms, so the lifespan, lipid and stress findings are preclinical and do not demonstrate human lifespan or healthspan benefits. The abstract does not report sample sizes, a comparison group, follow-up periods or statistical details.

Based on the study abstract; the full paper, tables and supplementary data were not reviewed.

Source & supporting passages

[1]
Perilla frutescens extract reduces fat accumulation and promotes longevity in Caenorhabditis elegans via modulation of the insulin/IGF-1 signaling pathway.

Huang L, Yin F, Fu X, Huang Y, Tang Y, Liao G, Wang B, Yang T, Huang G, Chen X. · europepmc.org · September 26, 2026

Read the quoted passagesIn the language of the original source
  1. Finding 1 ↑

    using Caenorhabditis elegans (C. elegans) as a
  2. Finding 2 ↑

    EAEPF markedly reduced lipid storage in nematodes
  3. Finding 3 ↑

    EAEPF activated the insulin/IGF-1 signaling (IIS) pathway

AI-assisted summary with linked source passages. No independent editorial or clinical review.

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