What question did this study set out to answer?

The aim is to investigate the antifibrotic effects and underlying mechanisms of kuwanon C in pulmonary fibrosis.

June 10, 2026Journal of Asian Natural Products Research0 citations

Kuwanon C alleviates pulmonary fibrosis via activation of the Nrf2 signaling pathway

QWQ WangCentral South University of Forestry and Technology TWTengfei WanCentral South University LRLu RenCentral South University

Key Points

The aim is to investigate the antifibrotic effects and underlying mechanisms of kuwanon C in pulmonary fibrosis.
Evaluated kuwanon C effects in a bleomycin-induced pulmonary fibrosis model.
Assessed TGF-β1-stimulated myofibroblast differentiation.
Measured histopathological injury, hydroxyproline accumulation, and fibrotic marker expression.
Kuwanon C alleviated pulmonary fibrosis and improved histopathological injury.
Significant reductions in hydroxyproline and fibrotic markers were observed.
Activation of the Nrf2 pathway was crucial, as silencing Nrf2 abolished protective effects.

Abstract

Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease lacking effective therapies. To investigate antifibrotic potential and mechanisms of kuwanon C, we evaluated its effects in bleomycin-induced IPF and TGF-β1-stimulated myofibroblast differentiation. Kuwanon C dose-dependently alleviated IPF, improved histopathological injury, reduced hydroxyproline accumulation and fibrotic marker expression, and suppressed TGF-β1-induced myofibroblast differentiation without cytotoxicity. Mechanistically, kuwanon C activated the Nrf2/HO-1/NQO-1 antioxidant pathway and attenuated oxidative stress, whereas Nrf2 silencing abolished these protective effects. These findings demonstrate that kuwanon C attenuates IPF by activating Nrf2 and inhibiting oxidative stress-driven fibroblast activation, highlighting its potential as a novel therapeutic candidate for IPF.

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