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<p>Atopic dermatitis (AD) is a chronic inflammatory skin disease. Salidroside, a major component of <i>Acer tegmentosum</i>, may be a valuable candidate for developing anti-AD agents. In this study, we investigated the therapeutic roles of salidroside and its related mechanisms in AD. For in vivo experiments, male BALB/c mice were challenged with 2,4-dinitrochlorobenzene (DNCB) to induce AD-like lesions and orally administered with salidroside for AD-like manifestations were induced by DNCB. Histological changes were assessed via hematoxylin-eosin staining and toluidine blue staining. Scratching numbers and spleen weight were evaluated. For in vitro experiments, TNF-α/IFN-γ-treated HaCaT cells and primary keratinocytes were used. Pro-inflammatory factors and pathway-associated proteins levels were measured by RT-qPCR and western blotting. Salidroside reduced the release of pro-inflammatory cytokines and chemokines in TNF-α/IFN-γ-treated HaCaT cells and primary keratinocytes. Salidroside alleviated DNCB-induced AD-like symptoms in mice. Salidroside attenuated the DNCB-induced atopic skin inflammation in vivo. Mechanistically, salidroside inactivated MAPK and NF-κB pathways in vitro and in vivo. Salidroside ameliorates AD-like responses via inactivating the MAPK and NF-κB pathways.</p>

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Salidroside alleviates atopic dermatitis-like responses by inhibiting MAPKs and NF-κB signaling pathways

  • 期刊论文

  • 发表日期：

    2025年4月1日

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  • Miaomiao Wang,
  • Yujie Xiong

摘要

Atopic dermatitis (AD) is a chronic inflammatory skin disease. Salidroside, a major component of Acer tegmentosum, may be a valuable candidate for developing anti-AD agents. In this study, we investigated the therapeutic roles of salidroside and its related mechanisms in AD. For in vivo experiments, male BALB/c mice were challenged with 2,4-dinitrochlorobenzene (DNCB) to induce AD-like lesions and orally administered with salidroside for AD-like manifestations were induced by DNCB. Histological changes were assessed via hematoxylin-eosin staining and toluidine blue staining. Scratching numbers and spleen weight were evaluated. For in vitro experiments, TNF-α/IFN-γ-treated HaCaT cells and primary keratinocytes were used. Pro-inflammatory factors and pathway-associated proteins levels were measured by RT-qPCR and western blotting. Salidroside reduced the release of pro-inflammatory cytokines and chemokines in TNF-α/IFN-γ-treated HaCaT cells and primary keratinocytes. Salidroside alleviated DNCB-induced AD-like symptoms in mice. Salidroside attenuated the DNCB-induced atopic skin inflammation in vivo. Mechanistically, salidroside inactivated MAPK and NF-κB pathways in vitro and in vivo. Salidroside ameliorates AD-like responses via inactivating the MAPK and NF-κB pathways.