Electrophilic PPARγ Ligands Attenuate IL-1β and Silica-Induced
Inflammatory Mediator Production in Human Lung Fibroblasts via a
PPARγ-Independent Mechanism
Figure 6
The PPAR antagonist GW9662 does not inhibit the anti-inflammatory effects of CDDO and 15d-PGJ2. Primary human lung fibroblasts were pretreated with 1 μM GW9662 for 3 hours, then PPAR ligands were added for 1 hour, then 1 ng/mL IL-1 was added for 24 hours. Supernatants were harvested and proinflammatory mediators were measured by ELISA or EIA. (a) IL-6, (b) MCP-1, (c) PGE2. Pretreatment with GW9662 did not significantly alter the attenuation of pro-inflammatory mediator production by CDDO or 15d-PGJ2 alone. Results are mean ± standard deviation for quadruplicate wells and are representative of 2 independent experiments that yielded similar results.
