ArticleClinical, cosmetic and investigational dermatology2024
Ergothioneine Protects Against UV-Induced Oxidative Stress Through the PI3K/AKT/Nrf2 Signaling Pathway.
Article in Clinical, cosmetic and investigational dermatology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The trial behind it
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Who cites it
8 citing papers in PubMed.
- Natural Histidine Derivatives-From Basic Research to Potential Applications in Cosmetics and Nutricosmetics.Antioxidants (Basel, Switzerland) · 2026Review
- Protein Post-Translational Modifications in UV-Induced Skin Damage.Experimental dermatology · 2026Review
- An integrated anti-aging framework targeting NADRedox biology · 2026Review
- Potential Protection Against Parkinson's Disease by Ergothioneine-Nature's Multifactorial Neuroprotectant.Antioxidants (Basel, Switzerland) · 2026Review
- Coordinated Regulation of Signaling Pathways by Stem Cell-Derived Extracellular Vesicles: A Promising Strategy Against Skin Photoaging.Clinical, cosmetic and investigational dermatology · 2026Review
- Biochemical Mechanism of Thai Fermented Soybean Extract on UVB-Induced Skin Keratinocyte Damage and Inflammation.International journal of molecular sciences · 2025Article
- The Current Situation and Future Trends of Ergothioneine in Biology and Medical Research: A Bibliometric Analysis.Journal of multidisciplinary healthcare · 2025Review
- Dysregulation of autophagy during photoaging reduce oxidative stress and inflammatory damage caused by UV.Frontiers in pharmacology · 2025Review
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Ergothioneine (EGT) is an antioxidant, which could be detected in human tissues, and human skin cells could utilize EGT and play an anti-oxidative role in keratinocytes. And in this study we are going to elucidate whether EGT could protect the skin from photoaging by Ultraviolet (UV) exposure in mice and its molecule pathway. Methods: Histological analysis was performed for evaluating the skin structure change. Malondialdehyde (MDA) and superoxide dismutase (SOD) levels were measured with biological assay for evaluating oxidative and antioxidative ability of skin exposed to UV light. And the level of marker molecules in mouse skin were detected by hydroxyproline (Hyp) assay, immunohistochemical analysis, Western blot, and quantitative real-time PCR (qRT-PCR). The markers of skin aging and cell death were tested by cell culture and treatment, Western blot and qRT-PCR. Results: EGT decreased the levels of inflammatory factors induced by UV exposure in mouse skin. MDA and SOD activity detection showed that EGT decreased MDA levels, increased SOD activity, and upregulated PI3K/Akt/Nrf2 signals in mouse skin exposed to UV, which further activated Nrf2 in the nucleus and enhanced the expression of Nrf2 target genes. In the cell model, we revealed that EGT could inhibit the increase in senescence-associated β-galactosidase-positive cells and p16 and γ-H2A.X positive cells induced by etoposide and activate PI3K/Akt/Nrf2 signaling. Moreover, a PI3K inhibitor blocked EGT protection against etoposide-induced cell death. Conclusion: The study showed EGT may play an important protective role against cell damage or death through the PI3K/Akt/Nrf2 signaling pathway in skin.
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