Therapeutic potential of sulforaphane throughout suppression of antimicrobial peptides in psoriatic HaCaT keratinocyte cells

Antimicrobial peptides (AMPs), such as β-defensin and S100 proteins, are known as innate immune functions that directly kill pathogens (bacteria) or activate macrophages to regulate the production of inflammatory cytokines and chemokines. However, AMPs are known to be overexpressed in psoriasis and...

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Bibliographic Details
Published in:Journal of applied biological chemistry 2024-12, Vol.67, p.380
Main Authors: Si Eun Park, Min Ji Kim, Hee Jun Kwon, Hyung Seo Hwang
Format: Article
Language:Korean
Subjects:
Anti-inflammation
Anti-microbial peptides
Cell counting kit-8
Psoriasis
Sulforaphane
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Summary:Antimicrobial peptides (AMPs), such as β-defensin and S100 proteins, are known as innate immune functions that directly kill pathogens (bacteria) or activate macrophages to regulate the production of inflammatory cytokines and chemokines. However, AMPs are known to be overexpressed in psoriasis and worsen the psoriatic lesion. Thus, we screened several compounds to discover natural psoriasis-regulating materials with effects on AMPs. Sulforaphane, contained in broccoli, is an isothiocyanate compound. Recently, the possibility of sulforaphane controlling psoriasis was reported partially in a study, but its antimicrobial peptide control function was not known at all. Thus, in this study, we investigated the AMPs inhibitory effect of sulforaphane using HaCaT cells induced by TNF-α, IL-17A, and IFN-γ. First, the maximum concentration affecting cytotoxicity was confirmed in TNF-α/IL-17A/IFN-γ stimulated HaCaT through a cell counting kit-8 cytotoxicity assay with sulforaphane at various concentrations. No cytotoxicity was observed at concentrations up to 2 μg/mL of sulforaphane in TNF-α/IL-17A/IFN-γ stimulated HaCaT for 2 h. First, the mRNA expression levels of AMPs such as β-defensin and S100A7 were all up-regulated in psoriatic cell model and sulforaphane significantly down-regulated its mRNA expression in same condition. Second, sulforaphane inhibited the mRNA gene expression of inflammatory cytokines IL-1β, IL-6, and chemokines C-C motif chemokine 20 and -X-C motif chemokine ligand 8 in TNF-α/IL-17A/IFN-γ stimulated HaCaT cells. Finally, sulforaphane alleviates psoriasis through inhibition of the IκB/NF- κB and STAT3 signaling pathways. These results suggest that sulforaphane shows potential in alleviating psoriatic symptoms by suppressing excessive AMPs and skin inflammation, and may be developed as an improvement material focused on psoriasis in the future.
ISSN:1976-0442