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

Sci Rep. 2023 Dec 15;13(1):22357. doi: 10.1038/s41598-023-49886-5.

Abstract

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.

MeSH terms

  • Epidermis* / metabolism
  • Humans
  • Inflammation / metabolism
  • Inflammation / prevention & control
  • Keratinocytes / metabolism
  • Mechanistic Target of Rapamycin Complex 1 / metabolism
  • Signal Transduction
  • Ultraviolet Rays / adverse effects
  • beta-Endorphin* / metabolism

Substances

  • beta-Endorphin
  • Mechanistic Target of Rapamycin Complex 1