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Research Article


 

Effects of Rosiglitazone oOf Rosiglitazone Oof page numbersdline styleompletely of the two inhibitorsn the Expression of PPAR-γ and the Production of IL-6 and IL-8 in Acute Lung Injury Model Using Human Pulmonary Epithelial Cells 

 

Sung Kyoung Kim, Chan Kwon Park, Sook Young Lee, Jeong Sup Song, Sung Hak Park, and Young Kyoon Kim*

Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, South Korea

 

For correspondence: E-mail: youngkim@catholic.ac.kr; Tel: +82-2-2258-6059; Fax: +82-2-596-2158


 

Received: 12 April 2011                                                                    Revised accepted: 22 September 2011

 

Tropical Journal of Pharmaceutical Research, Oct 2011; 10(5): 559-566

http://dx.doi.org/10.4314/tjpr.v10i5.4  

Abstract

 

Purpose: Peroxisome proliferator-activated receptor (PPAR)-γ ligand is known to repress the expression of pro-inflammatory mediators. However, it is unclear how it affects PPAR-γ expression and the inflammatory response in the human lung. We investigated the effects of rosiglitazone (synthetic PPAR-γ ligand) on the PPAR-γ expression and on the IL-6 and IL-8 production in acute lung injury model using human lung epithelial cells.

Methods: A549 and Beas-2B cells were pre-treated with rosiglitazone and/or BADGE (selective PPAR-γ antagonist) and then treated with media control or cytokine mixture including TNF-α, IL-1β, and IFN-γ. PPAR-γ expression was analyzed in cell lysates by Western blot. IL-6 and IL-8 production was measured in the culture supernatants by ELISA.

Results: PPAR-γ expression was identified in all experimental groups except for the control. The cytokine mixture-induced IL-6 and IL-8 production was significantly inhibited by pre-treatment with rosiglitazone (P<0.01). However, this inhibitory effect of rosiglitazone was not reversed by BADGE.

Conclusion: These suggest that rosiglitazone induces the PPAR-γ expression and it may inhibit the cytokine mixture-induced IL-6 and IL-8 production through the PPAR-γ independent pathway. The inhibitory mechanisms of rosiglitazone on the cytokine mixture-induced IL-6 and IL-8 production in human alveolar and bronchial epithelial cells remain to be further investigated.

 

Keywords: Rosiglitazone, PPAR-γ, IL-6, IL-8, Acute lung injury

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