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Phomopsterone B Alleviates Liver Fibrosis through mTOR-Mediated Autophagy and Apoptosis Pathway

Mei-Lin Peng1,2,3, Li-Jie Zhang1, Yan Luo1

  • 1State Key Laboratory of Functions and Applications of Medicinal Plants & School of Pharmacy, Guizhou Medical University, Guian New District, Guiyang 550004, China.

Molecules (Basel, Switzerland)
|January 23, 2024
PubMed

Insights

Phomopsterone B (PB) effectively reduces liver fibrosis by inhibiting hepatic stellate cell proliferation and promoting apoptosis. This compound targets the mTOR pathway, offering a potential new therapy for liver fibrosis.

Area of Science:

  • Pharmacology
  • Hepatology
  • Cell Biology

Background:

  • Liver fibrosis is a key pathological process in chronic liver diseases.
  • Targeting hepatic stellate cell (HSC) activation is a therapeutic strategy for liver fibrosis.
  • Phomopsterone B (PB) is a compound with potential therapeutic applications.

Purpose of the Study:

  • To investigate the anti-fibrotic activity of phomopsterone B (PB) in human hepatic stellate cells (HSCs).
  • To elucidate the underlying mechanism of PB's action in liver fibrosis.
  • To explore PB's effects on HSC proliferation, apoptosis, and autophagy.

Main Methods:

  • Human HSCs (LX-2 cells) were stimulated with TGF-β1.
  • PB treatment at various concentrations (1, 2, 4 μM).
  • Quantitative real-time PCR, Western blot, AO/EB staining, Hoechst33342 staining, flow cytometry, and assessment of autophagy markers (LC3B).
  • Investigation of the mTOR pathway using rapamycin and MHY1485.

Main Results:

  • PB significantly attenuated TGF-β1-induced HSC proliferation in a dose-dependent manner.
  • PB reduced the expression of fibrosis markers α-SMA and collagen I/III.
  • PB induced apoptosis and inhibited autophagy in HSCs.
  • PB's regulation of autophagy and apoptosis was mediated through the mTOR-dependent pathway.

Conclusions:

  • Phomopsterone B (PB) demonstrates significant anti-fibrotic effects in TGF-β1-stimulated human HSCs.
  • PB alleviates liver fibrosis by inhibiting HSC proliferation, promoting apoptosis, and modulating autophagy via the mTOR pathway.
  • PB represents a promising therapeutic candidate for the prevention and treatment of liver fibrosis.
Keywords:
apoptosisautophagyhepatic stellate cellsliver fibrosisphomopsterone B

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