Juglanin administration protects skin against UVB‑induced injury by reducing Nrf2‑dependent ROS generation
Affiliations: Department of Dermatology, the Affiliated Huaian No. 1 People's Hospital of Nanjing Medical University, Huai'an, Jiangsu 223300, P.R. China
- Published online on: April 24, 2020 https://doi.org/10.3892/ijmm.2020.4589
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Extensive solar ultraviolet B (UVB) exposure of the skin results in inflammation and oxidative stress, which may contribute to skin cancer. Natural products have attracted attention for their role in the effective treatment of cutaneous neoplasia. Juglanin is purified from the crude extract of Polygonum aviculare, exhibiting anti‑oxidant, anti‑inflammatory and anti‑cancer activities. Jugalanin was used in the current study to investigate whether it may ameliorate UVB irradiation‑induced skin damage by reducing oxidative stress and suppressing the inflammatory response in vivo and in vitro. In the present study, hairless mice were exposed to UVB irradiation in the absence or presence of juglanin administration for 10 weeks. The findings indicated that juglanin inhibited UVB‑induced hyperplasia and decreased infiltration in the skin of mice. UVB exposure‑induced oxidative stress in mice and cells was inhibited by juglanin via enhancing anti‑oxidant activity. Additionally, juglanin markedly reduced pro‑inflammatory cytokine release, including cyclic oxidase 2, interleukin‑1β and tumor necrosis factor‑α, triggered by chronic UVB irradiation. Juglanin‑ameliorated skin damage was associated with its suppression of mitogen activated protein kinases (MAPKs), including p38, extracellular signal regulated 1/2, and c‑Jun N‑terminal kinases, as well as nuclear factor (NF)‑κB signaling pathways, which was dependent on nuclear factor‑E2‑related factor 2 (Nrf2)‑modulated reactive oxygen species generation. Taken together, these data indicate that juglanin protected against UVB‑triggered oxidative stress and inflammatory responses by suppressing MAPK and NF‑κB activation via enhancing Nrf2 activity.