Level D· Scientific groundwork from lab and animal studiesAnimal StudyEurope PMCOpen access

Astragalus Polysaccharide Suppresses Inflammation and Promotes Apoptosis in Hypertrophic Scars by Suppressing OGT-Mediated Nrf2 O-GlcNAcylation

Wang H.

Animal Study on Chronic Wound, Scar, Chronic Inflammation, published in Iran J Pharm Res (2026) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
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Study type
Animal Study
Journal
Iran J Pharm Res (2026)
Reported sample size
—
Source database
Europe PMC
PMID
42157801
PMCID
PMC13181608
DOI
10.5812/ijpr-168614

Abstract (original English)

Background Hypertrophic scars (HS) arise from excessive tissue proliferation during wound healing, with Nrf2 involved, though the underlying mechanism remains unclear. Astragalus polysaccharides (APS) have anti-inflammatory and antioxidant properties, but their therapeutic effects and mechanisms in HS remain unreported. Objectives This study intends to clarify how APS target protein O-GlcNAcylation to treat HS. Methods A HS mouse model was established by subcutaneous injection of bleomycin (BLM) in C57BL/6 mice. Histopathology (H&E and Masson staining), ELISA, CCK-8, flow cytometry, western blot, and co-immunoprecipitation were performed to assess pathological changes, cell viability, apoptosis, inflammatory cytokine levels, and protein O-GlcNAcylation. Results Astragalus polysaccharides treatment significantly inhibited scar formation and reduced inflammatory cytokine levels in HS mice. In human hypertrophic scar fibroblasts (HHSFs), APS suppressed cell viability and inflammation while promoting apoptosis. Mechanistically, APS decreased global O-GlcNAcylation levels and downregulated the protein expression of OGT and Nrf2. Mechanistically, OGT interacted with Nrf2, enhancing its stability via O-GlcNAcylation at S199. Moreover, Nrf2 overexpression reversed APS-induced changes in HHSF viability, inflammation, and apoptosis. Conclusions This study identifies the OGT-mediated O-Gl

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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