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Peroxisome proliferator-activated receptor γ agonists reduce cell proliferation and viability and increase apoptosis
A Antonelli1, C Ferri, S M Ferrari
1Department of Internal Medicine, Metabolism Unit, University of Pisa School of Medicine, Via Roma 67, I-56100 Pisa, Italy. alessandro.antonelli@med.unipi.it
Background:
No study has evaluated the effect of the peroxisome proliferator-activated receptor γ (PPARγ) agonists on cell viability, proliferation and apoptosis in cultured systemic sclerosis (SSc) fibroblasts.
Objectives:
The effects of two pure PPARγ agonists (rosiglitazone and pioglitazone) in cultured SSc fibroblasts were evaluated and compared with effects in normal fibroblasts.
Methods:
The study included evaluation of cell viability and proliferation (based on the cleavage of tetrazolium salts and measurement of absorbance of the cell proliferation reagent WST-1), and determination of cell apoptosis (by means of the Hoechst dye uptake).
Results:
Rosiglitazone or pioglitazone (20μmolL(-1) ) significantly reduced cell proliferation (cell count of 75% and 83% compared with baseline, respectively, after 2h) and cell viability (absorbance reductions of 25% and 22% compared with baseline, respectively, after 2 h), and increased apoptosis (apoptotic cell percentages 9·9% and 8·6%, respectively, after 48h of incubation) in SSc fibroblasts, whereas they did not present a significant influence on control fibroblasts.
Conclusions:
The effects of rosiglitazone or pioglitazone shown on SSc fibroblasts raise the hypothesis of a therapeutic role for PPARγ agonists in patients affected by SSc.
Insights
Peroxisome proliferator-activated receptor γ (PPARγ) agonists, rosiglitazone and pioglitazone, reduced cell viability, proliferation, and increased apoptosis in systemic sclerosis (SSc) fibroblasts. This suggests a potential therapeutic role for PPARγ agonists in SSc treatment.
Area of Science:
- Fibroblast biology
- Cellular signaling pathways
- Connective tissue diseases
Background:
- Systemic sclerosis (SSc) is a complex autoimmune disease characterized by fibroblast activation and extracellular matrix deposition.
- The role of peroxisome proliferator-activated receptor γ (PPARγ) in SSc pathogenesis remains largely unexplored.
- No prior studies have investigated the impact of PPARγ agonists on SSc fibroblast behavior.
Purpose of the Study:
- To evaluate the effects of two pure PPARγ agonists, rosiglitazone and pioglitazone, on cultured SSc fibroblasts.
- To compare the effects of these agonists on SSc fibroblasts versus normal fibroblasts.
- To assess the impact of PPARγ agonists on cell viability, proliferation, and apoptosis in SSc fibroblasts.
Main Methods:
- Cell viability and proliferation were assessed using the WST-1 assay.
- Apoptosis was determined by Hoechst dye uptake.
- Experiments were conducted on cultured SSc fibroblasts and normal fibroblasts.
Main Results:
- Both rosiglitazone and pioglitazone significantly reduced cell proliferation and viability in SSc fibroblasts.
- These PPARγ agonists markedly increased apoptosis in SSc fibroblasts.
- Neither agonist demonstrated a significant effect on normal fibroblasts, highlighting SSc-specific responses.
Conclusions:
- The findings suggest that PPARγ agonists possess anti-fibrotic properties in the context of SSc.
- Rosiglitazone and pioglitazone demonstrate potential as therapeutic agents for systemic sclerosis.
- Further investigation into PPARγ agonist therapy for SSc is warranted based on these cellular effects.