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Published on: August 23, 2024

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

Tianxiang Qi1,2, Bingfeng Ma1,2, Yuanyuan Peng1,2

  • 1The 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.

Canadian Respiratory Journal
|June 28, 2026
PubMed

Insights

Cortex Mori Radicis (CMR) effectively treats pulmonary fibrosis (PF) by reducing inflammation and fibrosis. This traditional Chinese herb modulates the PI3K/AKT pathway, offering a potential multitargeted therapy for PF.

Area of Science:

  • Pharmacology
  • Traditional Chinese Medicine
  • Pulmonary Fibrosis Research

Background:

  • Pulmonary fibrosis (PF) involves persistent lung inflammation, fibroblast activation, and excessive extracellular matrix deposition.
  • Modulating inflammatory mediators is crucial for treating and preventing fibrotic lung diseases.
  • Cortex Mori Radicis (CMR), a traditional Chinese herb, possesses known anti-inflammatory and antifibrotic properties.

Purpose of the Study:

  • To investigate the therapeutic effects of Cortex Mori Radicis (CMR) on bleomycin-induced pulmonary fibrosis (PF).
  • To elucidate the underlying molecular mechanisms of CMR's action in PF treatment.
  • To explore CMR's potential as a multitargeted intervention for PF.

Main Methods:

  • In vivo studies using a bleomycin-induced PF mouse model.
  • In vitro experiments using A549 lung epithelial cells to assess migration, proliferation, and epithelial-mesenchymal transition (EMT).
  • Network pharmacological analysis to identify bioactive components and therapeutic targets, focusing on the PI3K/AKT pathway.
  • In vivo validation of PI3K/AKT pathway modulation by CMR.

Main Results:

  • CMR treatment significantly reduced inflammation and fibrosis in vivo, improving lung function.
  • In vitro, CMR inhibited A549 cell migration, proliferation, and EMT.
  • Network pharmacology identified 25 bioactive components and 10 targets, with the PI3K/AKT pathway as a key mechanism.
  • CMR administration suppressed PI3K/AKT pathway activation in vivo.

Conclusions:

  • Cortex Mori Radicis (CMR) demonstrates significant protective effects against pulmonary fibrosis (PF).
  • CMR acts by attenuating inflammation and fibrotic remodeling, primarily through modulation of the PI3K/AKT signaling pathway.
  • This study provides evidence for CMR's clinical potential in PF treatment, highlighting the benefits of traditional Chinese medicine's multitargeted approach.
Keywords:
Cortex Mori Radicisherbal medicinemolecular dockingnetwork pharmacologypulmonary fibrosis

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