Scholarlink

<p>Atopic dermatitis (AD) is a chronic inflammatory skin disorder marked by immune dysregulation and oxidative stress. Current therapies, such as corticosteroids, have side effects, necessitating new treatments. This study investigates the therapeutic effects of <i>Dendrobium officinale</i> polysaccharides (DOP) on AD, specifically focusing on their role in modulating inflammation and mitochondrial dysfunction. An AD-like model was induced in BALB/c mice, while HaCaT keratinocytes stimulated with TNF-α/IFN-γ served as an in vitro model. In mice, DOP significantly alleviated AD symptoms, reduced inflammatory cytokines (IL-1β, IL-6) and oxidative stress markers (MDA, NO), and restored antioxidant enzyme levels (GSH, SOD, CAT). In HaCaT cells, DOP ameliorated mitochondrial dysfunction, evident by increased mitochondrial membrane potential, cellular ATP content, and normalized mitochondrial dynamics (restoring MFN1/MFN2 and reducing DRP1). Furthermore, DOP suppressed NF-κB activation both in vivo and in vitro. These findings suggest that DOP alleviates AD by reducing inflammation and oxidative stress while preserving mitochondrial homeostasis. The mechanism appears associated with NF-κB inhibition, though this link is correlational and requires further direct validation.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Dendrobium officinale polysaccharides alleviate atopic dermatitis in vivo and in vitro through inhibition of inflammation and mitochondrial dysfunction

  • 期刊论文

  • 发表日期：

    2026年3月26日

查看全文
  • Bijun Zeng,
  • Gufen Jiang,
  • Chang Wang,
  • Hongxia Zhou,
  • Yujin Zhang,
  • Yi-ning Yan,
  • Zi Chen,
  • Lang Zhang,
  • Xiaoyu Li,
  • Mengzhou Xie,
  • Zhibo Yang,
  • Haizhen Wang

摘要

Atopic dermatitis (AD) is a chronic inflammatory skin disorder marked by immune dysregulation and oxidative stress. Current therapies, such as corticosteroids, have side effects, necessitating new treatments. This study investigates the therapeutic effects of Dendrobium officinale polysaccharides (DOP) on AD, specifically focusing on their role in modulating inflammation and mitochondrial dysfunction. An AD-like model was induced in BALB/c mice, while HaCaT keratinocytes stimulated with TNF-α/IFN-γ served as an in vitro model. In mice, DOP significantly alleviated AD symptoms, reduced inflammatory cytokines (IL-1β, IL-6) and oxidative stress markers (MDA, NO), and restored antioxidant enzyme levels (GSH, SOD, CAT). In HaCaT cells, DOP ameliorated mitochondrial dysfunction, evident by increased mitochondrial membrane potential, cellular ATP content, and normalized mitochondrial dynamics (restoring MFN1/MFN2 and reducing DRP1). Furthermore, DOP suppressed NF-κB activation both in vivo and in vitro. These findings suggest that DOP alleviates AD by reducing inflammation and oxidative stress while preserving mitochondrial homeostasis. The mechanism appears associated with NF-κB inhibition, though this link is correlational and requires further direct validation.