Photobiomodulation attenuates corticosterone-induced neuronal injury via activation of the AMPK/ULK1 signaling pathway.
Near-infrared light protected cultured neuronal cells from several corticosterone-related stress signals. This is early laboratory work and does not show that PBM treats stress-related conditions in people.
Li N, Ma C, Zhou T, Li N, Deng W, Ye Y, Liu Y, Chen H.
Journal of photochemistry and photobiology. B, Biology · Publication date: 2026-09-15
Added to site: 2026-09-20
DOI: 10.1016/j.jphotobiol.2026.113565
Electronic publication date verified in Europe PMC.
- Modalities
- Photobiomodulation, Near-infrared light
- Clinical focus
- Neuronal stress, Mitochondrial function, Autophagy
- Population
- Cell model of corticosterone-related neuronal injury, not humans or whole animals
- Sample
- Mouse hippocampal HT22 cells exposed to corticosterone
- Intervention / method
- Optimized 808 nm PBM followed by cell-viability, oxidative-stress, inflammatory, mitochondrial, apoptosis and autophagy-related assays; the AMPK inhibitor Compound C tested pathway involvement
- Comparator
- Corticosterone-exposed cells with and without PBM, plus pharmacological AMPK inhibition
Clinician summary
PBM improved viability, oxidative, inflammatory, mitochondrial and apoptosis measures in corticosterone-treated HT22 cells. AMPK inhibition attenuated much of the response, supporting an AMPK-ULK1 and autophagy-related mechanism for further study.
How to interpret the findings
This was an in-vitro mouse-cell model with no human participants, behavioral outcomes, tissue penetration test or clinical comparator. Optimized dish-level exposure and pharmacological pathway inhibition do not establish a safe or effective human protocol.
Equipment and disclosures
The cell experiment used 808 nm PBM; the device model and complete irradiation parameters were not available in the checked abstract.
Funding and competing-interest details were not available in the checked indexed record.
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Summary prepared with AI assistance. Source verification does not imply an independent replication or a clinician's endorsement. Read our review method.