Cortex Mori Radicis Mitigates Inflammation and Fibrosis in Pulmonary Fibrosis Through PI3K/AKT Pathway Suppression

  • Can Respir J. 2026;2026(1):e8459298. doi: 10.1155/carj/8459298.
Tianxiang Qi  1  2 ,  Bingfeng Ma  1  2 ,  Yuanyuan Peng  1  2 ,  Yafeng Liu  1  2 ,  Jianqiang Guo  1  2 ,  Xingyu Yang  1  2 ,  Xuansheng Ding  1  3 ,  Dingfei Ren  4 ,  Dong Hu  2  5
Affiliations
  • 1. The First Affiliated Hospital of Anhui University of Science and Technology (Huainan First People's Hospital), School of Medicine, Anhui University of Science and Technology, Huainan, China, aust.edu.cn.
  • 2. Anhui Occupational Health and Safety Engineering Laboratory, School of Medicine, Anhui University of Science and Technology, Huainan, China, aust.edu.cn.
  • 3. School of Pharmacy, China Pharmaceutical University, Nanjing, China, cpu.edu.cn.
  • 4. Occupational Control Hospital of Huaihe Energy Group, Huainan, China.
  • 5. Key Laboratory of Industrial Dust Deep Reduction and Occupational Health and Safety of Anhui Higher Education Institutes, School of Medicine, Anhui University of Science and Technology, Huainan, China, aust.edu.cn.
PMID: 42365453 DOI: 10.1155/carj/8459298
Abstract

Early in the pathogenesis of pulmonary fibrosis (PF), there are multiple inflammatory cell infiltrations in the damaged lung tissue. When lung injury persists, inflammatory cytokines prompt local fibroblasts migration and hyperproliferation, triggering abnormal deposition of extracellular matrix in the lung interstitium. This excessive repair leads to interstitial cell reorganization, triggering lung tissue fibrosis and further activation of inflammatory cells. Therefore, modulation of inflammatory mediators is of great significance in the treatment and prevention in the process of fibrosis. Cortex Mori Radicis (CMR) is a traditional Chinese herb with anti-inflammatory and antifibrotic properties. In this study, we investigated the therapeutic effects of CMR on bleomycin-induced PF using in vivo and in vitro models. In vivo experiments showed that CMR treatment significantly reduced inflammation, attenuated fibrosis, and alleviated lung function decline. In vitro, CMR inhibited migration, proliferation, and epithelial-mesenchymal transition (EMT) in A549 lung epithelial cells. Network pharmacological analysis identified 25 bioactive components and 10 key therapeutic targets in CMR, with the PI3K/Akt signaling pathway emerging as the core regulatory mechanism. Subsequent in vivo validation confirmed that CMR could inhibit the activation of the PI3K/Akt pathway. In conclusion, CMR exerts protective effects against PF by modulating the PI3K/Akt pathway, thereby attenuating inflammation and fibrotic remodeling. This study provides both pharmacodynamic evidence and mechanistic insight supporting the clinical potential of CMR and underscores the advantages of multitargeted intervention strategies offered by traditional Chinese medicine in the treatment of PF.

Keywords
Cortex Mori Radicis; herbal medicine; molecular docking; network pharmacology; pulmonary fibrosis.
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