PPAR-γagonists inhibit TGF-β1-induced chemokine expression in human tubular epithelial cells

• 来源期刊: 中国药理学报（英文版）
• 关键词: peroxisome proliferator-activated receptor-γ 15d-PGJ2 troglitazone transforming growth factor β1 tubular epithelial cell chemokine monocyte chemoattractant protein-1 interleukin-8
• 年，卷（期）: 2009,（1）
• 页码范围: 107-112
• 页数: 6页
• 语种: 英文
• DOI: 10.1038/aps.2008.15

摘要

Aim: Peroxisome proliferator-activated receptor-γ (PPAR-γ) has a wide range of biological functions, including anti-inflam-mation. In this study, we investigated the inhibitory effects of PPAR-γ on transforming growth factor [β1 (TGF-β1)-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-β1. Expression of MCP-1 and IL-8 was measured using real-time PCR and ELISA. Results: Treatment with 5 ng/mL TGF-β1 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 μmol/L and TGL at 2.5 μmol/L exhibited inhibitory effects on TGF-β1-induced MCP-1 expres-sion. Additionally, 15d-PGJ2 at 2.5 and 5 μmol/L and TGL at 2.5 μmol/L inhibited TGF-β1-induced expression of IL-8. Conclusion: PPAR-γ agonists (15d-PGJ2 and TGL) could inhibit the TGF-β1-induced expression of chemokines in HK-2 cells. Our results suggest that PPAR-γ agonists have the potential to be used as a treatment regimen to reduce inflamma-tion in renal tubulointerstitial disease.