PL-ReliefTMplus Alleviates Atopic Dermatitis and Regulates Inflammatory Responses via Inhibiting NF-κB Signaling Pathway

Chem Biodivers. 2024 Aug;21(8):e202400349. doi: 10.1002/cbdv.202400349. Epub 2024 Jul 9.

Abstract

Background: Atopic dermatitis (AD) has various detrimental effects on individuals with limited drug cure rates which necessitate the development of new treatment methods. PL-ReliefTMplus (PLR) is composed of SupraOlive, Crocus Sativus extracts and Citrus reticulata extracts. The effect of PLR on AD remains to be explored.

Methods: 2,4-dinitrofluorobenzene-induced AD model mice were involved and the histopathology of the skin lesions was observed along with the levels of inflammatory chemokines levels were measured. To further validate the molecular mechanism of PLR, RNA-seq was performed in HaCaT cells. Western blotting and immunofluorescence were performed to investigate NF-κB signaling pathways response in AD.

Results: Due to PLR treatment, the thickening of the epidermis and dermis was inhibited and the number of eosinophils, mast cells, and CD4+ T cells in the skin lesion was decreased. In addition, the levels of inflammatory cytokines were decreased in dorsal skin tissues and LPS-stimulated HaCat cells. Furthermore, KEGG pathway analysis suggested that most identified downstream biological functions were associated with inflammatory response. PLR inhibited NF-κB signaling in AD mice and HaCaT cells.

Conclusions: These results indicate that PLR is a potent therapeutic agent for attenuating symptoms of AD.

Keywords: Atopic dermatitis; HaCaT cells; NF-κB signaling; SupraOlive.

MeSH terms

  • Animals
  • Citrus / chemistry
  • Cytokines / metabolism
  • Dermatitis, Atopic* / chemically induced
  • Dermatitis, Atopic* / drug therapy
  • Dermatitis, Atopic* / metabolism
  • Dermatitis, Atopic* / pathology
  • Dinitrofluorobenzene
  • Disease Models, Animal
  • HaCaT Cells
  • Humans
  • Inflammation / chemically induced
  • Inflammation / drug therapy
  • Inflammation / metabolism
  • Inflammation / pathology
  • Mice
  • Mice, Inbred BALB C
  • NF-kappa B* / antagonists & inhibitors
  • NF-kappa B* / metabolism
  • Plant Extracts / chemistry
  • Plant Extracts / pharmacology
  • Signal Transduction* / drug effects

Substances

  • NF-kappa B
  • Plant Extracts
  • Dinitrofluorobenzene
  • Cytokines