%0 Journal Article
%T Effects of Rosiglitazone on the Expression of PPAR-¦Ã and the Production of IL-6 and IL-8 in Acute Lung Injury Model Using Human Pulmonary Epithelial Cells
%A SK Kim
%A CK Park
%A SY Lee
%A JS Song
%A SH Park
%A YK Kim
%J Tropical Journal of Pharmaceutical Research
%D 2011
%I University of Benin
%X Purpose: Peroxisome proliferator-activated receptor (PPAR)-¦Ã ligand is known to repress the expression of pro-inflammatory mediators. However, it is unclear how it affects PPAR-¦Ã expression and the inflammatory response in the human lung. We investigated the effects of rosiglitazone (synthetic PPAR-¦Ã ligand) on the PPAR-¦Ã 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-¦Ã antagonist) and then treated with media control or cytokine mixture including TNF-¦Á, IL-1 ¦Â, and IFN-¦Ã. PPAR-¦Ã 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-¦Ã 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-¦Ã expression and it may inhibit the cytokine mixture-induced IL-6 and IL-8 production through the PPAR-¦Ã 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.
%U http://www.ajol.info/index.php/tjpr/article/view/71658