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<p>Apigetrin (7-(β-<span>d</span>-glucopyranosyloxy)-4′,5-dihydroxyflavone) is a phytochemical abundant in chamomile. It exhibits potent biological activities, including anti-inflammatory, pro-autophagic, and anticancer effects, while offering superior solubility. However, until recently, little was known about activity of apigetrin on skin regulation, including its effects on psoriasis. First, we compared the cytotoxicity of apigetrin with other polyphenol compounds, such as quercetin and luteolin, to confirm its excellent safety. Apigetrin downregulated the mRNA of inflammatory cytokines, including interleukin-1α/β (IL-1α/β), IL-6, and C-X-C motif chemokine ligand 8 (CXCL8), in HaCaT keratinocyte cells stimulated with tumor necrosis factor-α (TNF-α)/interferon-γ (IFN-γ)/IL-17A at nontoxic concentrations. Apigetrin significantly suppressed intracellular signaling factors, such as I kappa B (IκB) and Signal transducer and activator of transcription 3 (STAT3), in a dose-dependent manner. In addition, apigetrin increased the resistance value in a dose-dependent manner in the Transendothelial Electrical Resistance (TEER) assay. It also increased the expression of cornified envelope proteins, such as loricrin (LOR), and significantly inhibited MMP-9 expression, suggesting that it restores the skin barrier. Finally, we found that apigetrin significantly inhibited the expression of IL-1α, IL-6, and C–C motif chemokine ligand 20 (CCL20) as well as MMP-9 mRNA in the dermal fibroblast Hs68 cell model. The above results show apigetrin not only improves the skin barrier of the epidermis but also exhibits excellent anti-inflammatory effects in a dermis cell model.</p>

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Apigetrin ameliorates psoriatic inflammation and skin barrier dysfunction via NF-κB/STAT3 pathway in epidermal and dermal cell models

  • 期刊论文

  • 发表日期：

    2026年7月27日

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  • Jung Hyun Lee,
  • Min Ji Kim,
  • Hyung Seo Hwang

摘要

Apigetrin (7-(β-d-glucopyranosyloxy)-4′,5-dihydroxyflavone) is a phytochemical abundant in chamomile. It exhibits potent biological activities, including anti-inflammatory, pro-autophagic, and anticancer effects, while offering superior solubility. However, until recently, little was known about activity of apigetrin on skin regulation, including its effects on psoriasis. First, we compared the cytotoxicity of apigetrin with other polyphenol compounds, such as quercetin and luteolin, to confirm its excellent safety. Apigetrin downregulated the mRNA of inflammatory cytokines, including interleukin-1α/β (IL-1α/β), IL-6, and C-X-C motif chemokine ligand 8 (CXCL8), in HaCaT keratinocyte cells stimulated with tumor necrosis factor-α (TNF-α)/interferon-γ (IFN-γ)/IL-17A at nontoxic concentrations. Apigetrin significantly suppressed intracellular signaling factors, such as I kappa B (IκB) and Signal transducer and activator of transcription 3 (STAT3), in a dose-dependent manner. In addition, apigetrin increased the resistance value in a dose-dependent manner in the Transendothelial Electrical Resistance (TEER) assay. It also increased the expression of cornified envelope proteins, such as loricrin (LOR), and significantly inhibited MMP-9 expression, suggesting that it restores the skin barrier. Finally, we found that apigetrin significantly inhibited the expression of IL-1α, IL-6, and C–C motif chemokine ligand 20 (CCL20) as well as MMP-9 mRNA in the dermal fibroblast Hs68 cell model. The above results show apigetrin not only improves the skin barrier of the epidermis but also exhibits excellent anti-inflammatory effects in a dermis cell model.