Electrophilic PPARγ Ligands Attenuate IL-1β and Silica-Induced
Inflammatory Mediator Production in Human Lung Fibroblasts via a
PPARγ-Independent Mechanism
Figure 2
The PPAR ligands are not overtly cytotoxic at the doses used. (a) Primary human lung fibroblasts were treated for 24 hours with the indicated concentrations of CDDO, or 15d-PGJ2 (PGJ2), and LDH released into the media was measured by commercial LDH activity assay. There were no significant differences between any of the treatment groups compared to MEM control. Results are mean ± standard deviation for triplicate wells and are representative of 2 independent experiments that yielded similar results. (b) Primary human lung fibroblasts were plated in a 96-well plate and treated with the indicated concentrations of CDDO or 15d-PGJ2 (PGJ2). Cell viability was determined after 24 hours by MTT assay. The results shown are the mean ± standard deviation of quadruplicate wells and are normalized to untreated control wells.
