<p>Ultraviolet B (UVB) is a major external factor causing ultraviolet damage. This study assessed the protective effects of <i>Dendrobium officinale </i>polysaccharides (DOP) from both stems and leaves on UVB-induced skin damage in HaCaT Human Keratinocytes. Notably, stem DOPs (DOP1J, DOP3J, and DOP8J) outperformed leaf DOPs (DOP1Y, DOP3Y, and DOP8Y) in mitigating UVB-induced damage, with DOP1J and DOP8J demonstrating the highest efficacy in preserving cell proliferation. The DOPs exhibited antioxidant properties by enhancing superoxide dismutase, catalase, and glutathione peroxidase activities, and reducing reactive oxygen species levels. They curtailed cellular aging by inhibiting UVB-induced protein phosphorylation of p38, JNK, and ERK1/2 within the mitogen-activated protein kinase (MAPK) signaling pathway and by suppressing the protein expression of p53 and matrix metalloproteinases (MMPs, including MMP-1 and MMP-9). The mechanism underlying DOPs’ protective effects appears to be a dual-action approach: bolstering antioxidant defenses and dampening the MAPK pathway’s activation, thereby hindering the expression of MMPs.</p> Graphical abstract <p></p>

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Dendrobium officinale polysaccharides: alleviating UVB-induced skin damage by anti-oxidation and inhibiting matrix metalloproteinases expression

  • Zhejie Xu,
  • Wanyi Zhou,
  • Chenchen Yang,
  • Ni Zhang,
  • Jingrui Li,
  • Wenyang Tao,
  • Jianrong Xing,
  • Ying Yang,
  • Yali Dang

摘要

Ultraviolet B (UVB) is a major external factor causing ultraviolet damage. This study assessed the protective effects of Dendrobium officinale polysaccharides (DOP) from both stems and leaves on UVB-induced skin damage in HaCaT Human Keratinocytes. Notably, stem DOPs (DOP1J, DOP3J, and DOP8J) outperformed leaf DOPs (DOP1Y, DOP3Y, and DOP8Y) in mitigating UVB-induced damage, with DOP1J and DOP8J demonstrating the highest efficacy in preserving cell proliferation. The DOPs exhibited antioxidant properties by enhancing superoxide dismutase, catalase, and glutathione peroxidase activities, and reducing reactive oxygen species levels. They curtailed cellular aging by inhibiting UVB-induced protein phosphorylation of p38, JNK, and ERK1/2 within the mitogen-activated protein kinase (MAPK) signaling pathway and by suppressing the protein expression of p53 and matrix metalloproteinases (MMPs, including MMP-1 and MMP-9). The mechanism underlying DOPs’ protective effects appears to be a dual-action approach: bolstering antioxidant defenses and dampening the MAPK pathway’s activation, thereby hindering the expression of MMPs.

Graphical abstract