Electrophilic PPARγ Ligands Attenuate IL-1β and Silica-Induced
Inflammatory Mediator Production in Human Lung Fibroblasts via a
PPARγ-Independent Mechanism
Figure 5
PPAR ligands attenuate IL-1-induced PGE2 production in human lung fibroblasts. Primary human lung fibroblasts were pretreated with 20 μM rosiglitazone (Rosi), 1 μM CDDO, or 5 μM 15d-PGJ2 (PGJ2) and then cotreated with IL-1 for 24 hours as previously described. Supernatants were harvested, and PGE2 was determined by EIA. PGE2 production is significantly reduced in PPAR ligand-treated fibroblasts compared to IL-1 alone (*). CDDO and 15d-PGJ2 were significantly more potent than rosiglitazone (†). Results are mean ± standard deviation for quadruplicate wells and are representative of 3 independent experiments that yielded similar results. Data were analyzed by ANOVA.
