TY - JOUR
T1 - Saccharomyces/pearl ferment lysate filtrate repairs UVB-induced skin barrier damage by regulating Nrf2/HO-1 and JNK/MAPK signaling pathways
AU - Liu, Tanglin
AU - Guo, Biao
AU - Tong, Liying
AU - Li, Hao
AU - Wang, Caibing
AU - Zang, Kai
AU - Zhao, Ruili
AU - Zhao, Xinyi
AU - Ye, Chenglong
AU - Ye, Xiyun
AU - Dang, Yongyan
N1 - Publisher Copyright:
© 2026 Elsevier B.V.
PY - 2026/2
Y1 - 2026/2
N2 - Pearls have skin whitening and antioxidant properties, but their effects on skin barrier are less understood. This study investigated the reparative effects of saccharomyces/pearl ferment lysate filtrate (PFL) on UVB-induced skin barrier damage. In HaCaT cells, PFL restored proteins related to epidermal differentiation, tight junctions, and moisture retention, all reduced by UVB exposure, and lowered the expression of inflammatory factors. Similarly, in a UVB-induced skin damage mouse model, PFL significantly alleviated skin peeling, erythema, TWEL and epidermal thickening, while also suppressing UVB-induced skin inflammation. Mechanistically, PFL promoted Nrf2 nuclear translocation and upregulated antioxidant proteins NQO1 and HO-1, hereby decreasing ROS accumulation. It also inhibited the activation of the c-Jun N-terminal kinase (JNK) pathway in response to UVB-induced oxidative stress, likely due to the activation of Nrf2. These findings indicate that PFL may repair UVB-induced skin barrier damage through activation of the Nrf2/HO-1 pathway and inhibition of the JNK/MAPK pathway, offering potential as a therapeutic agent for skin barrier repair.
AB - Pearls have skin whitening and antioxidant properties, but their effects on skin barrier are less understood. This study investigated the reparative effects of saccharomyces/pearl ferment lysate filtrate (PFL) on UVB-induced skin barrier damage. In HaCaT cells, PFL restored proteins related to epidermal differentiation, tight junctions, and moisture retention, all reduced by UVB exposure, and lowered the expression of inflammatory factors. Similarly, in a UVB-induced skin damage mouse model, PFL significantly alleviated skin peeling, erythema, TWEL and epidermal thickening, while also suppressing UVB-induced skin inflammation. Mechanistically, PFL promoted Nrf2 nuclear translocation and upregulated antioxidant proteins NQO1 and HO-1, hereby decreasing ROS accumulation. It also inhibited the activation of the c-Jun N-terminal kinase (JNK) pathway in response to UVB-induced oxidative stress, likely due to the activation of Nrf2. These findings indicate that PFL may repair UVB-induced skin barrier damage through activation of the Nrf2/HO-1 pathway and inhibition of the JNK/MAPK pathway, offering potential as a therapeutic agent for skin barrier repair.
KW - Inflammation
KW - MAPK
KW - Nrf2
KW - Saccharomyces/pearl ferment lysate filtrate
KW - Skin barrier damage
KW - UVB
UR - https://www.scopus.com/pages/publications/105027397995
U2 - 10.1016/j.jphotobiol.2026.113366
DO - 10.1016/j.jphotobiol.2026.113366
M3 - 文章
AN - SCOPUS:105027397995
SN - 1011-1344
VL - 275
JO - Journal of Photochemistry and Photobiology B: Biology
JF - Journal of Photochemistry and Photobiology B: Biology
M1 - 113366
ER -