ArticleScientific reports2026
Epimedin C attenuates airway inflammation and remodeling in Asthma by intervening M2 macrophage polarization via modulating the PI3K/Akt/mTOR signaling pathway.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.
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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.
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Corrections and comments
- Erratum issued
- Erratum issued
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9 authors.
Funding
Abstract
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.
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