Cycloastragenol extended lifespan in C. elegans via insulin signaling and p38 MAPK immunity
In the nematode Caenorhabditis elegans, 0.2 μM Cycloastragenol extended mean lifespan by 30.64% and improved aging-related traits; the abstract attributes this to a telomerase-independent mechanism involving inhibition of insulin/IGF-1 signaling and activation of a p38 MAPK immune axis. [1]
Automatic summary · not editorially reviewed
The key findings
In Caenorhabditis elegans, 0.2 μM Cycloastragenol was identified as the optimal concentration and extended mean lifespan by 30.64%. [1]
CAG treatment improved locomotion, reduced lipofuscin accumulation, improved stress resistance and strengthened immunity against Pseudomonas aeruginosa. [1]
The authors report the first evidence that CAG acts through a telomerase-independent mechanism inhibiting the IIS pathway and activating the p38 MAPK axis. [1]
The source at a glance
- Study type / format
- Preclinical experimental study in an animal model (abstract)
- Population / context
- Caenorhabditis elegans nematodes in a laboratory study
- Summary based on
- Study abstract
- Original publication
- September 10, 2026
C. elegans test of a Astragalus triterpenoid
The abstract describes a study in the nematode Caenorhabditis elegans testing Cycloastragenol (CAG), a bioactive triterpenoid from Astragalus membranaceus. The authors note that CAG is known for telomerase activation but that its non-telomeric mechanisms needed clarification. They identified 0.2 μM as the optimal concentration, which extended mean lifespan by 30.64%. This is an animal-model experiment, not evidence of a human lifespan effect.
Supporting source [1]
Aging traits and immune defense in the worms
According to the abstract, CAG treatment ameliorated aging-associated phenotypes: locomotion improved, lipofuscin accumulation was reduced, stress resistance improved and immunity against Pseudomonas aeruginosa was strengthened. Mechanistic analyses reported nuclear translocation of the FOXO transcription factor DAF-16 and elevated antioxidant enzyme activities. Using mutant strains and gene expression profiling, the authors report the first evidence that CAG acts through a telomerase-independent mechanism, simultaneously inhibiting the Insulin/IGF-1 Signaling (IIS) pathway and activating the p38 MAPK (SEK-1/PMK-1/SKN-1) axis.
Supporting source [1]
Abstract-only scope and preclinical limits
The abstract links CAG-mediated innate immune enhancement to longevity and distinguishes this mode of action from earlier telomere-centric models. It states that the findings clarify the pharmacological basis of CAG and support its potential development as a therapeutic agent for age-related disorders. These are preclinical results in a nematode; the abstract does not report human data, and the full text was not reviewed. The described associations and mechanisms do not establish that CAG extends human lifespan or prevents disease.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Results come from the nematode Caenorhabditis elegans, a preclinical model, and the abstract reports no human data. The described associations and mechanisms do not establish human lifespan or disease-prevention benefits.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Feng C, Zhang X, Zhao T, Shi T, Zhao P, Wang M, Ren J, Xu K, Yao J, Zhang L, Yin X, Xia X. · europepmc.org · September 10, 2026