Parishin B from Gastrodia elata extended lifespan in C. elegans and reduced senescence markers in cells
In the abstract, parishin B, a phenolic constituent of Gastrodia elata, extended mean lifespan in wild-type C. elegans by 23.88% at 200 μM and improved stress resistance and proteotoxicity phenotypes; mammalian cell experiments also showed protection and reduced senescence-associated phenotypes. [1]
Automatic summary · not editorially reviewed
The key findings
The study used C. elegans as an in vivo model, with lifespan, stress resistance and transgenic disease-model assays, plus transcriptomic, reporter and genetic approaches. [1]
At 200 μM, parishin B produced a 23.88% increase in mean lifespan of wild-type C. elegans. [1]
In mammalian cells, parishin B protected PC12 cells against Aβ 1-42-induced cytotoxicity and attenuated senescence-associated phenotypes in mouse embryonic fibroblasts. [1]
The source at a glance
- Study type / format
- Preclinical in vivo and cell-model study (abstract)
- Population / context
- Wild-type and transgenic Caenorhabditis elegans, PC12 cells and mouse embryonic fibroblasts.
- Summary based on
- Study abstract
- Original publication
- September 23, 2026
Parishin B tested in nematodes and mammalian cells
The abstract describes an in vivo study using Caenorhabditis elegans, with lifespan assays, lifespan-related phenotypic analyses, stress resistance assays and transgenic models of neurodegenerative diseases. Transcriptomic profiling, quantitative RT-PCR, fluorescent reporter analyses and genetic approaches were used to identify signaling pathways. Effects on cellular senescence and neurotoxicity were further evaluated in mammalian cell models.
Supporting source [1]
Lifespan gain and stress resistance in C. elegans
Parishin B significantly extended the lifespan of wild-type C. elegans, with 200 μM producing a 23.88% increase in mean lifespan. It improved locomotor activity, muscle integrity, mitochondrial morphology, lipid homeostasis and lipofuscin accumulation. It also alleviated proteotoxicity-associated phenotypes in nematode models of Alzheimer's, Parkinson's and Huntington's disease. The abstract states that parishin B requires DAF-16/FOXO, SKN-1/Nrf2, HSF-1 and HLH-30 for its cytoprotective effects.
Supporting source [1]
Mammalian cell results and abstract-only scope
In mammalian systems, parishin B protected PC12 cells against Aβ 1-42-induced cytotoxicity and attenuated senescence-associated phenotypes in mouse embryonic fibroblasts. The abstract concludes that parishin B activates conserved stress-response and proteostasis-regulating pathways. These are preclinical findings in nematodes and cultured cells; the abstract does not report human lifespan, clinical outcomes or safety data.
Supporting source [1]
How to interpret this
This explainer is based on the abstract only; the full text was not reviewed. Findings come from C. elegans and cultured mammalian cells, not from human studies, and the abstract reports no clinical outcomes or safety data.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Shi L, Liu YL, Fu HH, Luo HR, Wu GS. · europepmc.org · September 23, 2026