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<p>Incontinence-associated dermatitis (IAD) is a prevalent inflammatory skin condition caused by prolonged exposure to urine and feces, particularly in elderly and critically ill patients. The pathogenesis of IAD is closely linked to chronic inflammation, which results in the excessive release of pro-inflammatory cytokines and skin barrier dysfunction. This study investigates the therapeutic potential of quercetin, a natural flavonoid with known anti-inflammatory and antioxidant properties, in a rat model of IAD. We found that quercetin (50–100&#xa0;mg/kg) downregulated the expression and phosphorylation of IKKα/β and NF-κB by over 40%, leading to a marked reduction (approximately 40–70%) in pro-inflammatory cytokines (TNF-α, IL-6, IL-1β and IFN-γ). Furthermore, quercetin promoted skin barrier repair, as evidenced by about one-fold improvement in transepidermal water loss measurements and nearly three-fold increase in filaggrin expression. Histological findings showing enhanced epidermal integrity, reduced inflammatory cell infiltration and suppressed cell apoptosis. Our findings suggest that quercetin mitigates inflammation and accelerates skin barrier repair in IAD by targeting the IKK/NF-κB pathway, offering a promising therapeutic strategy for this debilitating condition.</p>

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Quercetin alleviates incontinence-associated dermatitis via IKK/NF-κB pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月30日

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  • Yan Zhang,
  • Ge Zhao,
  • Junfang Duan,
  • Dajiang Yuan,
  • Chenli Xu,
  • Lijuan Song,
  • Yinghui Zhang

摘要

Incontinence-associated dermatitis (IAD) is a prevalent inflammatory skin condition caused by prolonged exposure to urine and feces, particularly in elderly and critically ill patients. The pathogenesis of IAD is closely linked to chronic inflammation, which results in the excessive release of pro-inflammatory cytokines and skin barrier dysfunction. This study investigates the therapeutic potential of quercetin, a natural flavonoid with known anti-inflammatory and antioxidant properties, in a rat model of IAD. We found that quercetin (50–100 mg/kg) downregulated the expression and phosphorylation of IKKα/β and NF-κB by over 40%, leading to a marked reduction (approximately 40–70%) in pro-inflammatory cytokines (TNF-α, IL-6, IL-1β and IFN-γ). Furthermore, quercetin promoted skin barrier repair, as evidenced by about one-fold improvement in transepidermal water loss measurements and nearly three-fold increase in filaggrin expression. Histological findings showing enhanced epidermal integrity, reduced inflammatory cell infiltration and suppressed cell apoptosis. Our findings suggest that quercetin mitigates inflammation and accelerates skin barrier repair in IAD by targeting the IKK/NF-κB pathway, offering a promising therapeutic strategy for this debilitating condition.