Open Access

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

  • Authors:
    • Xiao‑Qing Li
    • Li‑Min Cai
    • Jing Liu
    • Yan‑Li Ma
    • Ying‑Hui Kong
    • He Li
    • Ming Jiang
  • View Affiliations

  • Published online on: June 5, 2018     https://doi.org/10.3892/ijmm.2018.3720
  • Pages: 1445-1459
  • Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

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 vivo and in vitro using SKH‑1 hairless mice and HACAT cells, respectively. The animals were exposed to UVB irradiation (180 mJ/cm2) 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 vivo 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.
View Figures
View References

Related Articles

Journal Cover

September-2018
Volume 42 Issue 3

Print ISSN: 1107-3756
Online ISSN:1791-244X

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Li XQ, Cai LM, Liu J, Ma YL, Kong YH, Li H and Jiang M: 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. Int J Mol Med 42: 1445-1459, 2018.
APA
Li, X., Cai, L., Liu, J., Ma, Y., Kong, Y., Li, H., & Jiang, M. (2018). 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. International Journal of Molecular Medicine, 42, 1445-1459. https://doi.org/10.3892/ijmm.2018.3720
MLA
Li, X., Cai, L., Liu, J., Ma, Y., Kong, Y., Li, H., Jiang, M."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". International Journal of Molecular Medicine 42.3 (2018): 1445-1459.
Chicago
Li, X., Cai, L., Liu, J., Ma, Y., Kong, Y., Li, H., Jiang, M."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". International Journal of Molecular Medicine 42, no. 3 (2018): 1445-1459. https://doi.org/10.3892/ijmm.2018.3720