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Objective <p>Wound healing requires fibroblast activation, including proliferation, migration, and extracellular matrix (ECM) remodeling. Astragalus polysaccharides (APs), derived from Astragalus membranaceus, have been reported to promote tissue repair, but the underlying mechanisms remain unclear. This study examined whether APs facilitate wound healing through the miR-92a/FGF2 axis.</p> Methods <p>Human foreskin fibroblasts (HFF-1) were incubated with APs, and proliferation, migration, FGF2, and miR-92a expression were evaluated. Functional assays involved miR-92a overexpression or inhibition. A full-thickness skin defect rat model was utilized to assess wound closure and molecular changes following AP treatment with or without miR-92a agomir.</p> Results <p>APs enhanced fibroblast proliferation and migration, increased FGF2 expression, and suppressed miR-92a levels. miR-92a directly targeted FGF2, thereby inhibiting fibroblast activity. Overexpression of miR-92a weakened the pro-healing effects of APs, whereas inhibition restored them. In rats, APs accelerated wound closure and elevated FGF2 expression, while miR-92a agomir impaired repair and reduced FGF2 expression.</p> Conclusion <p>APs promote cutaneous wound repair by modulating the miR-92a/FGF2 axis, with miR-92a acting as a negative regulator. Targeting this pathway may strengthen the therapeutic potential of APs in skin regeneration.</p> Graphical abstract <p></p>

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Astragalus polysaccharide accelerates wound healing by targeting the miR-92a/FGF2 axis in dermal fibroblasts

  • 期刊论文

  • 发表日期：

    2026年5月2日

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  • Zexing Tang,
  • Kang Han,
  • Shisong Sang,
  • Shusen Tan,
  • Haitao Meng,
  • Yan Liang,
  • Donghui Bian

摘要

Objective

Wound healing requires fibroblast activation, including proliferation, migration, and extracellular matrix (ECM) remodeling. Astragalus polysaccharides (APs), derived from Astragalus membranaceus, have been reported to promote tissue repair, but the underlying mechanisms remain unclear. This study examined whether APs facilitate wound healing through the miR-92a/FGF2 axis.

Methods

Human foreskin fibroblasts (HFF-1) were incubated with APs, and proliferation, migration, FGF2, and miR-92a expression were evaluated. Functional assays involved miR-92a overexpression or inhibition. A full-thickness skin defect rat model was utilized to assess wound closure and molecular changes following AP treatment with or without miR-92a agomir.

Results

APs enhanced fibroblast proliferation and migration, increased FGF2 expression, and suppressed miR-92a levels. miR-92a directly targeted FGF2, thereby inhibiting fibroblast activity. Overexpression of miR-92a weakened the pro-healing effects of APs, whereas inhibition restored them. In rats, APs accelerated wound closure and elevated FGF2 expression, while miR-92a agomir impaired repair and reduced FGF2 expression.

Conclusion

APs promote cutaneous wound repair by modulating the miR-92a/FGF2 axis, with miR-92a acting as a negative regulator. Targeting this pathway may strengthen the therapeutic potential of APs in skin regeneration.

Graphical abstract