Electrophilic PPARγ Ligands Attenuate IL-1β and Silica-Induced
Inflammatory Mediator Production in Human Lung Fibroblasts via a
PPARγ-Independent Mechanism
Figure 7
A strong electrophilic carbon is necessary for PPAR ligand-mediated attenuation of inflammation in IL-1-treated human lung fibroblasts. Primary human lung fibroblasts were pretreated with 1 μM CDDO, 5 μM 15d-PGJ2 (PGJ2), 5 μM CAY10410, (CAY) or 15 μM PGA1 for 1 hour and then co-treated with 1 ng/mL of IL-1 for 24 hours. Supernatants were harvested, and cytokine concentrations were measured by ELISA. (a) CDDO, 15d-PGJ2, and PGA1, but not CAY10410, significantly inhibited production of IL-6 (*). (b) CDDO, 15d-PGJ2, PGA1, and CAY10410 all significantly reduced MCP-1 production (*). CDDO, 15d-PGJ2, and PGA1 were significantly more potent than CAY10410 (†). Results are mean ± standard deviation for quadruplicate wells and are representative of 3 independent experiments.
