β-endorphin suppresses ultraviolet B irradiation-induced epidermal barrier damage by regulating inflammation-dependent mTORC1 signaling

Solar ultraviolet B (UVB) radiation triggers excessive inflammation, disrupting the epidermal barrier, and can eventually cause skin cancer. A previous study reported that under UVB irradiation, epidermal keratinocytes synthesize the proopiomelanocortin-derived peptide β-endorphin, which is known fo...

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Bibliographic Details
Published in:Scientific reports 2023-12, Vol.13 (1), p.22357-22357, Article 22357
Main Authors: Kim, Hyung-Su, Kim, Hyoung-June, Hong, Yong-Deog, Son, Eui Dong, Cho, Si-Young
Format: Article
Language:English
Subjects:
631/80
631/80/86
631/80/86/2366
AKT protein
Analgesics
beta-Endorphin - metabolism
Endorphins
Epidermis - metabolism
Humanities and Social Sciences
Humans
Inflammation
Inflammation - metabolism
Inflammation - prevention & control
Irradiation
Keratinocytes
Keratinocytes - metabolism
Mechanistic Target of Rapamycin Complex 1 - metabolism
multidisciplinary
NF-κB protein
Proopiomelanocortin
Radiation
Science
Science (multidisciplinary)
Signal Transduction
Skin cancer
TOR protein
Ultraviolet radiation
Ultraviolet Rays - adverse effects
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Summary:Solar ultraviolet B (UVB) radiation triggers excessive inflammation, disrupting the epidermal barrier, and can eventually cause skin cancer. A previous study reported that under UVB irradiation, epidermal keratinocytes synthesize the proopiomelanocortin-derived peptide β-endorphin, which is known for its analgesic effect. However, little is known about the role of β-endorphin in UVB-exposed skin. Therefore, in this study, we aimed to explore the protective role of β-endorphin against UVB irradiation-induced damage to the skin barrier in normal human keratinocytes (NHKs) and on a human skin equivalent model. Treatment with β-endorphin reduced inflammatory responses in UVB-irradiated NHKs by inactivating the NF-κB signaling pathway. Additionally, we found that β-endorphin treatment reversed UVB-induced abnormal epidermal proliferation and differentiation in NHKs and, thus, repaired the skin barrier in UVB-treated skin equivalents. The observed effects of β-endorphin on UVB-irradiated NHKs were mediated via blockade of the Akt/mTOR signaling pathway. These results reveal that β-endorphin might be useful against UVB-induced skin injury, including the disruption of the skin barrier function.
ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-023-49886-5