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Updated: Jan 8, 2026
An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
Published on: June 6, 2025
Sanmiao pill ameliorates rheumatoid arthritis via PPARγ-mediated lipid accumulation in macrophage: A multi-omics and
Quanao Jiang1, Xiaoman Jiang2, Shi Lin Xia2
1School of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine, Hefei 230012, China; Key Laboratory of Xin'an Medicine, Ministry of Education, Hefei 230038, China.
Background:
The enhanced infiltration of M1-polarized macrophages into synovium acts as a central driver of chronic inflammation characteristics of rheumatoid arthritis (RA). Sanmiao pill (SMP), a classic traditional formulation, has long been employed in the treatment of arthralgia syndromes. Despite its recognized therapeutic efficacy, the underlying mechanism remains unclear.
Purpose:
To explore the therapeutic potential and protective mechanisms of SMP against RA.
Methods:
A collagen-induced arthritis (CIA) rat model was established, the therapeutic effects were evaluated by arthritis severity, immune organ status, histopathological and ultrasound examination. A chinmedomics approach-integrating serum medicinal chemistry, network pharmacology, lipidomics, proteomics, immunofluorescence, western blotting and molecular docking, was used for the systematic elucidation of SMP's mechanism.
Results:
A total of 11 migration compounds derived from SMP were identified in serum, representing potential pharmacodynamic substances responsible for its anti-RA effects. Pharmacodynamic evaluation revealed that SMP effectively alleviated chronic synovitis associated with macrophages polarization imbalance. SMP also improved synovial lipid deposition, along with a trend toward normalization of the serum lipid profiles. Integrated analysis from network pharmacology, lipidomics and proteomics indicated that SMP may exert its effects by modulating PPARγ-mediated lipid metabolism disorders. In vitro, SMP suppressed macrophages M1 polarization, accompanied by a decrease in lipid droplet formation and PGE2 release. Notably, these effects were caused by the up-regulation of PPARγ, with immunofluorescence providing support for SMP-induced nuclear translocation of PPARγ.
Conclusion:
SMP alleviated RA synovitis by promoting PPARγ nuclear translocation, which subsequently restrained lipid droplet accumulation and PGE2 release, and in turn limited macrophages M1 polarization.
Insights
Sanmiao pill (SMP) treats rheumatoid arthritis (RA) by reducing M1 macrophage infiltration and inflammation. It works by promoting PPARγ nuclear translocation, which limits lipid accumulation and inflammatory mediator release in the synovium.
Area of Science:
- Rheumatology
- Immunology
- Pharmacology
Background:
- Rheumatoid arthritis (RA) is driven by M1 macrophage infiltration into the synovium.
- Sanmiao pill (SMP) is a traditional remedy for arthralgia, but its RA treatment mechanism is unknown.
Purpose of the Study:
- To investigate the therapeutic effects and mechanisms of SMP in rheumatoid arthritis.
Main Methods:
- A collagen-induced arthritis (CIA) rat model was used to assess SMP's efficacy.
- A chinmedomics approach, integrating multiple omics and molecular techniques, elucidated SMP's mechanism of action.
Main Results:
- SMP treatment reduced RA severity, synovitis, and immune organ abnormalities.
- SMP modulated macrophage polarization, improved lipid metabolism, and normalized lipid profiles by up-regulating PPARγ.
- In vitro studies confirmed SMP's suppression of M1 polarization and inflammatory mediator release via PPARγ activation.
Conclusions:
- SMP alleviates RA synovitis by enhancing PPARγ nuclear translocation.
- This mechanism limits lipid deposition and PGE2 release, thereby reducing M1 macrophage polarization and inflammation.
