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<p>In bronchial asthma, M2 macrophage polarization and PI3K/Akt/mTOR pathway activation are critically implicated in airway inflammation and remodeling. This study employed an OVA-induced asthmatic mouse model to evaluate the therapeutic effect of Epimedin C, a major flavonoid from Herba Epimedii with reported anti-inflammatory and immunoregulatory effects. Pulmonary function tests, histological staining, ELISA, RT-qPCR, and western blotting were utilized to assess airway responsiveness, inflammation, and remodeling. The mechanisms involving the PI3K/Akt/mTOR pathway and macrophage polarization were further investigated via flow cytometry and immunofluorescence. Results showed that Epimedin C significantly improved lung function and alleviated pathological changes. These therapeutic effects were accompanied by suppression of PI3K/Akt/mTOR phosphorylation and inhibition of M2 polarization. Further mechanistic investigation confirmed that M2 polarization was dependent on PI3K/Akt/mTOR activation. Inhibiting this pathway can reverse M2 hyperpolarization and reduce pro-inflammatory mediator production. In conclusion, Epimedin C may alleviate asthma by suppressing M2 macrophage polarization through inhibition of the PI3K/Akt/mTOR pathway. These findings may offer a novel understanding of Epimedin C treatment and furnish evidence for an alternative therapeutic approach to asthma.</p>

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Epimedin C attenuates airway inflammation and remodeling in Asthma by intervening M2 macrophage polarization via modulating the PI3K/Akt/mTOR signaling pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月16日

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  • Zewen Zhang,
  • Shoubao Cao,
  • Ziwen Qin,
  • Tingting Liu,
  • Qin He,
  • Gen Li,
  • Chuanjun Huang,
  • Yujuan Chen,
  • Yunshan Wang

摘要

In bronchial asthma, M2 macrophage polarization and PI3K/Akt/mTOR pathway activation are critically implicated in airway inflammation and remodeling. This study employed an OVA-induced asthmatic mouse model to evaluate the therapeutic effect of Epimedin C, a major flavonoid from Herba Epimedii with reported anti-inflammatory and immunoregulatory effects. Pulmonary function tests, histological staining, ELISA, RT-qPCR, and western blotting were utilized to assess airway responsiveness, inflammation, and remodeling. The mechanisms involving the PI3K/Akt/mTOR pathway and macrophage polarization were further investigated via flow cytometry and immunofluorescence. Results showed that Epimedin C significantly improved lung function and alleviated pathological changes. These therapeutic effects were accompanied by suppression of PI3K/Akt/mTOR phosphorylation and inhibition of M2 polarization. Further mechanistic investigation confirmed that M2 polarization was dependent on PI3K/Akt/mTOR activation. Inhibiting this pathway can reverse M2 hyperpolarization and reduce pro-inflammatory mediator production. In conclusion, Epimedin C may alleviate asthma by suppressing M2 macrophage polarization through inhibition of the PI3K/Akt/mTOR pathway. These findings may offer a novel understanding of Epimedin C treatment and furnish evidence for an alternative therapeutic approach to asthma.