Figure 12.

(A) A TransAM™ PPARγ transcription factor assay was used to assess PPARγ activity in nuclear extracts of DHA (10 μM) and PPARγ agonist rosiglitazone (10 μM) treated RAW-ASC cells. Data presented as mean ± SEM, n = 2. Asterisks indicate significant relative to the control (*p < 0.05, **p < 0.01). (B) RAW-ASC cells were incubated in serum-deprived RPMI containing DHA (10 μM), rosiglitazone (10 μM), PPARγ antagonist SR16832 (100 nM), or VEH (BSA) for 24 h. Cultures were then incubated with 20 ng/ml LPS for 3.5 h. Assessment of mRNA levels by qRT-PCR showed that the PPARγ antagonist SR16832 blocked DHA and rosiglitazone-dependent suppression of LPS-induced gene expression. Gene expression represented as copy number relative to Gapdh. Asterisks indicate significant differences between DHA and BSA treated cells (*p < 0.05, **p < 0.01). Data presented as mean ± SEM, n = 3. Different letters indicate significant differences between treatment groups within VEH treated cells (uppercase letters) or SR16832 treated cells (lowercase letters) (p < 0.05). Representative of two independent experiments.