Electrophilic PPARγ Ligands Attenuate IL-1β and Silica-Induced
Inflammatory Mediator Production in Human Lung Fibroblasts via a
PPARγ-Independent Mechanism
Figure 4
Immunofluorescence of human lung fibroblasts demonstrates CDDO and 15d-PGJ2 attenuate IL-1β-induced COX-2 expression. Fibroblasts were pretreated with PPAR agonists for 1 hour prior to IL-1 (1 ng/mL) treatment for 24 hours. Cells were fixed and permeabilized and probed for COX-2 protein. COX-2 was visualized with Alexa Fluor 488 (green) and cell nuclei with DAPI (blue). (a) MEM control; (b) IL-1; (c) IL-1 + 20 μM rosiglitazone; (d) IL-1 + 1 μM CDDO; (e) IL-1 + 5 M 15d-PGJ2, (f) IL-1 + 5 M CAY10410. IL-1-induced COX-2 was inhibited by CDDO (d) and 15d-PGJ2 (e).
