Juglanin administration protects skin against UVB‑induced injury by reducing Nrf2‑dependent ROS generation

胡桃苷给药可通过减少 Nrf2 依赖性 ROS 生成来保护皮肤免受 UVB 引起的损伤

阅读:5
作者:Ying-Hui Kong, Su-Ping Xu

Abstract

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.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。