AI Article Synopsis
- The study explored the role of PPAR-gamma in inhibiting inflammatory markers (IL-8 and MCP-1) in renal cells induced by TGF-beta1.
- HK-2 cells were treated with compounds 15d-PGJ2 and troglitazone (TGL) to assess their effects on gene expression and protein levels of these chemokines.
- Results showed that both compounds effectively reduced TGF-beta1-induced chemokine expression, suggesting potential use in reducing inflammation in kidney diseases.
Article Abstract
Aim: Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) has a wide range of biological functions, including anti-inflammation. In this study, we investigated the inhibitory effects of PPAR-gamma on transforming growth factor beta1 (TGF-beta1)-induced interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) expression in renal tubular epithelial cells (HK-2).
Methods: HK-2 cells were pretreated with 15d-PGJ2 or troglitazone (TGL) and then treated with TGF-beta1. Expression of MCP-1 and IL-8 was measured using real-time PCR and ELISA.
Results: Treatment with 5 ng/mL TGF-beta1 for 24 h increased both MCP-1 and IL-8 mRNA and protein levels in HK-2 cells. Both 15d-PGJ2 at 2.5 and 5 micromol/L and TGL at 2.5 micromol/L exhibited inhibitory effects on TGF-beta1-induced MCP-1 expression. Additionally, 15d-PGJ2 at 2.5 and 5 micromol/L and TGL at 2.5 micromol/L inhibited TGF-beta1-induced expression of IL-8.
Conclusion: PPAR-gamma agonists (15d-PGJ2 and TGL) could inhibit the TGF-beta1-induced expression of chemokines in HK-2 cells. Our results suggest that PPAR-gamma agonists have the potential to be used as a treatment regimen to reduce inflammation in renal tubulointerstitial disease.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4006532 | PMC |
| http://dx.doi.org/10.1038/aps.2008.15 | DOI Listing |
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