Open AccessSambucus nigra L. ameliorates UVB-induced photoaging and inflammatory response in human skin keratinocytes
Author(s) -
Pei Lin,
Eunson Hwang,
Hien T. T. Ngo,
Seul A Seo,
TaeHoo Yi
Publication year - 2019
Publication title -
cytotechnology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.488
H-Index - 62
eISSN - 1573-0778
pISSN - 0920-9069
DOI - 10.1007/s10616-019-00342-1
Subject(s) - photoaging , inflammation , mapk/erk pathway , signal transduction , chemistry , reactive oxygen species , oxidative stress , human skin , pharmacology , skin aging , kinase , cancer research , biochemistry , biology , immunology , medicine , dermatology , genetics
Sambucus nigra L. (Elderberry) is widely used as a dietary supplement in functional food and possesses many pharmacological activities to prevent ailments, such as the colds and fever, diabetes and cancer. However, research on its skin anti-aging effect is still limited. Here, we evaluated the recovery effects of elderberry extract (EB) in UVB-irradiated human skin keratinocytes (HaCaTs) and investigated whether EB represents a potential therapeutic agent against skin photoaging and inflammation. In this study, EB showed good efficiency on scavenging free radicals and dose-dependently reduced reactive oxygen species (ROS) generation. EB notably decreased UVB-induced matrix metalloproteinase-1 (MMP-1) expression and inflammatory cytokine secretion through the inhibition of mitogen-activated protein kinases/activator protein 1 (MAPK/AP-1) and nuclear factor-κB (NF-κB) signaling pathways, blocking extracellular matrix (ECM) degradation and inflammation in UVB-irradiated HaCaTs. In addition, EB improved nuclear factor E2-related factor 2/heme oxygenase-1 (Nrf2/HO-1) signaling to increase oxidative defense capacity, and enhanced transforming growth factor beta (TGF-β) signaling activation to promote procollagen type I synthesis, relieving UVB-induced skin cell damage. These results indicated that EB has the potential to ameliorate UVB-induced skin photoaging and inflammation.