Evidence map›Paper›PMID 42157801›Full record

ArticleIranian journal of pharmaceutical research : IJPR

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

Hengfei Wang

Abstract read
In one paragraph

Article in Iranian journal of pharmaceutical research : IJPR. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

1 author.

Hengfei WangMedical College of Hexi University, Zhangye, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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-GlcNAcylation of Nrf2 as a novel regulatory mechanism in HS progression. By suppressing this axis, APS demonstrates therapeutic potential for HS. These findings highlight O-GlcNAcylation as a promising therapeutic target and support the clinical development of APS for fibrotic skin disorders.

Indexed as

Astragalus PolysaccharidesHypertrophic ScarNrf2O-GlcNAcylation

Identifiers

PMID42157801
PMCPMC13181608

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