Liquiritin suppresses UVB-induced skin injury through prevention of inflammation, oxidative stress and apoptosis through the TLR4/MyD88/NF-κB and MAPK/caspase signaling pathways

Solar ultraviolet B (UVB) radiation is known to trigger inflammation, oxidative stress and apoptotic responses through various signaling pathways, which eventually lead to skin cancer. The present study investigated whether liquiritin suppresses UVB-induced skin injury in viv and in vitr using SKH-1 hairless mice and HACAT cells, respectively. The animals were exposed to UVB irradiation (180 mJ/cm(2)) for 20 min, followed by liquiritin treatment. The findings indicated that UVB exposure resulted in the excessive release of pro-inflammatory cytokines, including interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-18, IL-6 and cyclooxygenase (COX)2, which were dependent on the toll-like receptor (TLR)4/myeloid differentiation factor 88 (MyD88)/nuclear factor-κB (NF-κB) signaling pathway. Oxidative stress was also observed, evidenced by reduced antioxidants and elevated oxidants. Apoptosis, examined using terminal deoxynucleotidyl transferase dUTP nick end labeling and crystal violet staining, suggested that UVB irradiation caused cell death in viv and in vitro, which was closely associated with p38/c-Jun N-terminal kinase and caspase activity. Of note, liquiritin treatment in mice and cells exposed to UVB showed reduced inflammatory response, oxidative stress and apoptosis through inhibiting the activation of TLR4/MyD88/NF-κB mitogen-activated protein kinases and caspase pathways, and downregulating the release of oxidants. Overall, the data revealed that liquiritin may be a useful compound against UVB-induced skin injury.