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

  • J Asian Nat Prod Res. 2026 Jun 8:1-16. doi: 10.1080/10286020.2026.2680649.
Qian Wang  1  2  3  4 ,  Teng-Fei Wan  5 ,  Lu Ren  6  7 ,  Zun Wang  2 ,  Si-Yuan Tang  2  3
Affiliations
  • 1. Clinical Nursing Teaching and Research Section, The Second Xiangya Hospital of Central South University, Changsha 410011, China.
  • 2. School of Nursing, Ningxia Medical University, Yinchuan 750004, China.
  • 3. Xiangya school of Nursing, Central South University, Changsha 410013, China.
  • 4. Department of Psychiatry, National Clinical Research Center for Mental Disorders, and National Center for Mental Disorders, The Second Xiangya Hospital of Central South University, Changsha 410011, China.
  • 5. Department of Orthopedics, Xiangya Hospital of Central South University, Changsha 410008, China.
  • 6. Department of Dermatology, The Second Xiangya Hospital of Central South University, Changsha 410000, China.
  • 7. Department of Nursing, The Second Xiangya Hospital of Central South University, Changsha 410011, China.
PMID: 42257653 DOI: 10.1080/10286020.2026.2680649
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.

Keywords
Kuwanon C; Nrf2; myofibroblast differentiation; oxidative stress; pulmonary fibrosis.
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