Swertianin Suppresses M1 Macrophage Polarization and Inflammation in Metabolic Dysfunction-Associated Fatty Liver

Jing Xia1,2, Wei Xiong1,2, Ce Yang1,3

  • 1Chongqing Key Laboratory of Development and Utilization of Genuine Medicinal Materials in Three Gorges Reservoir Area, Chongqing 404120, China.

Genes
|June 26, 2025
PubMed

Insights

Swertianin effectively treats metabolic dysfunction-associated fatty liver disease (MASLD) by activating PPARG. This action reduces macrophage inflammation and lipid accumulation, improving liver health.

Area of Science:

  • Pharmacology
  • Hepatology
  • Immunology

Background:

  • Metabolic dysfunction-associated fatty liver disease (MASLD) involves immune dysregulation and macrophage inflammation.
  • PPARG activation is crucial for macrophage polarization and lipid metabolism in MASLD.
  • PPARG represents a potential therapeutic target for MASLD.

Purpose of the Study:

  • To investigate Swertia davidi Franch components and targets using UPLC-Q/TOF-MS and network pharmacology.
  • To evaluate the therapeutic potential of Swertianin for MASLD.
  • To elucidate Swertianin's mechanism involving PPARG activation and macrophage modulation.

Main Methods:

  • Utilized UPLC-Q/TOF-MS and network pharmacology to identify key compounds and targets of Swertia davidi Franch.
  • Conducted in vitro macrophage experiments to assess M1 polarization modulation.
  • Employed a mouse model of MASLD to evaluate Swertianin's therapeutic efficacy.

Main Results:

  • Swertianin activated PPARG, significantly inhibiting M1 macrophage polarization.
  • Observed reduced lipid accumulation and decreased inflammatory markers in vitro and in vivo.
  • Demonstrated significant improvement in liver pathology in MASLD mouse models.

Conclusions:

  • Swertianin activates PPARG, offering a novel therapeutic mechanism for MASLD.
  • The study highlights Swertianin's potential to target macrophage polarization and inflammation in MASLD.
  • Swertianin shows promise as a treatment for MASLD by modulating key inflammatory pathways.