Electrophilic PPARγ Ligands Attenuate IL-1β and Silica-Induced
Inflammatory Mediator Production in Human Lung Fibroblasts via a
PPARγ-Independent Mechanism
Figure 3
CDDO and 15d-PGJ2 attenuate IL-1-induced COX-2 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) for 1 hour and then cotreated with 1 ng/mL of IL-1 for 24 hours. Protein lysates were harvested and Western blot analysis was performed by probing for protein expression of COX-2 and GAPDH (for normalization). (a) Representative samples are shown. (b) Quadruplicate samples were analyzed by densitometry and normalized to GAPDH. COX-2 expression was significantly reduced in CDDO and 15d-PGJ2 treated cells 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.
