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Objective <p>Allergic asthma is a chronic airway inflammatory disease with limited therapeutic options in clinical practice. Ethyl ferulate (EF), a natural compound commonly found in <i>Chuanxiong</i>, <i>Danggui</i> and grains, has been shown to possess multiple biological activities. However, the effect of EF on allergic asthma and its underlying mechanisms remains unclear. This study aimed to investigate the therapeutic potential and mechanism of EF in allergic asthma.</p> Methods <p>The house dust mite (HDM)-induced allergic asthma mouse model was used to evaluate the effects of EF on airway inflammation and macrophage M2 polarization. Adoptive transfer experiments were used to confirm the critical role of M2 polarization in the attenuation of allergic asthma by EF. Mechanistic studies were performed by using IL-4-stimulated RAW264.7 cells and bone marrow-derived macrophages (BMDMs).</p> Results <p>EF significantly attenuated HDM-induced airway inflammation, eosinophil infiltration, mucus secretion, and airway remodeling. EF suppressed M2 macrophage markers (CD206, Arg1, Ym1, Fizz1) in lung tissues and IL-4-stimulated macrophages. Mechanistically, EF blocked STAT6 phosphorylation and nuclear translocation, thereby inhibiting the STAT6/IRF4 pathway.</p> Conclusions <p>EF alleviates allergic asthma by inhibiting M2 macrophage polarization via disruption of the STAT6/IRF4 signaling pathway, supporting its potential as a therapeutic agent derived from traditional medicine.</p>

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Ethyl ferulate attenuates allergic asthma via inhibiting macrophage M2 polarization through STAT6/IRF4 pathway

  • 期刊论文

  • 发表日期：

    2026年6月29日

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  • Longlong Ge,
  • Weizhen Chen,
  • Shuguang Han,
  • Huan Yang,
  • Mingchen Du,
  • Shengpeng Li,
  • Xinran Bai,
  • Peilin Zhao,
  • Dan Chen,
  • Qingfeng Pang,
  • Yaxian Wu

摘要

Objective

Allergic asthma is a chronic airway inflammatory disease with limited therapeutic options in clinical practice. Ethyl ferulate (EF), a natural compound commonly found in Chuanxiong, Danggui and grains, has been shown to possess multiple biological activities. However, the effect of EF on allergic asthma and its underlying mechanisms remains unclear. This study aimed to investigate the therapeutic potential and mechanism of EF in allergic asthma.

Methods

The house dust mite (HDM)-induced allergic asthma mouse model was used to evaluate the effects of EF on airway inflammation and macrophage M2 polarization. Adoptive transfer experiments were used to confirm the critical role of M2 polarization in the attenuation of allergic asthma by EF. Mechanistic studies were performed by using IL-4-stimulated RAW264.7 cells and bone marrow-derived macrophages (BMDMs).

Results

EF significantly attenuated HDM-induced airway inflammation, eosinophil infiltration, mucus secretion, and airway remodeling. EF suppressed M2 macrophage markers (CD206, Arg1, Ym1, Fizz1) in lung tissues and IL-4-stimulated macrophages. Mechanistically, EF blocked STAT6 phosphorylation and nuclear translocation, thereby inhibiting the STAT6/IRF4 pathway.

Conclusions

EF alleviates allergic asthma by inhibiting M2 macrophage polarization via disruption of the STAT6/IRF4 signaling pathway, supporting its potential as a therapeutic agent derived from traditional medicine.