Open Access

Wound healing effect of an Astragalus membranaceus polysaccharide and its mechanism

  • Authors:
    • Bingjiang Zhao
    • Xuanfen Zhang
    • Wei Han
    • Ju Cheng
    • Yonghong Qin
  • View Affiliations

  • Published online on: April 20, 2017     https://doi.org/10.3892/mmr.2017.6488
0

Abstract

In the present study, a novel polysaccharide, APS2-1, was isolated and purified from Astragalus membranaceus using DEAE-cellulose and Sephadex G-100 chromatography. The effect of APS2‑1 on the promotion of wound healing was evaluated and its preliminary mechanism was investigated. In vitro experiments showed that APS2‑1 was able to promote human skin fibroblast (HSF) propagation and accelerate cell cycle progression. For further examination, a scalded mice model was used to verify the effect of APS2‑1 and investigate its mechanism of action. The analysis of biochemical parameters, including cyclin D1, inhibitor of nuclear factor κBα (IκBα), transforming growth factor (TGF)‑β1, basic fibroblast growth factor (bFGF) and epidermal growth factor (EGF) showed that APS2‑1 inhibited the increase in cyclin D1 and IκBα, and promoted the expression of TGF‑β1, bFGF and EGF, which was further confirmed by histopathological observation. These results suggested that APS2‑1 possessed high potential in wound healing and its mechanism was associated with inhibiting inflammation, accelerating cell cycle and promoting the secretion of repair factors.

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Print ISSN: 1791-2997
Online ISSN:1791-3004

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APA
Zhao, B., Zhang, X., Han, W., Cheng, J., & Qin, Y. (1899). Wound healing effect of an Astragalus membranaceus polysaccharide and its mechanism. Molecular Medicine Reports, 0, 0-0. https://doi.org/10.3892/mmr.2017.6488
MLA
Zhao, B., Zhang, X., Han, W., Cheng, J., Qin, Y."Wound healing effect of an Astragalus membranaceus polysaccharide and its mechanism". Molecular Medicine Reports 0.0 (1899): 0-0.
Chicago
Zhao, B., Zhang, X., Han, W., Cheng, J., Qin, Y."Wound healing effect of an Astragalus membranaceus polysaccharide and its mechanism". Molecular Medicine Reports 0, no. 0 (1899): 0-0. https://doi.org/10.3892/mmr.2017.6488