• peroxisome proliferator-activated receptor gamma (PPARγ);
  • bisphenol A diglycidyl ether (BADGE);
  • lipopolysaccharide (LPS);
  • tumor necrosis factor-α (TNF-α);
  • nuclear factor-kappaB (NF-κB);
  • coactivator

Bisphenol A diglycidyl ether (BADGE) is a newly described peroxisome proliferator-activated receptor γ (PPARγ) antagonist in adipogenic cells. In contrast, in the macrophage-like cell line RAW 264.7, BADGE, like the PPARγ agonist pioglitazone hydrochloride, not only increased promoter activity of the PPARγ-luciferase reporter gene, but also suppressed lipopolysaccharide (LPS)-induced tumor necrosis factor-α (TNF-α) production. These results suggest that BADGE is a PPARγ agonist in RAW 264.7 cells. Furthermore, overexpression of the coactivator p300 restored BADGE- or pioglitazone hydrochloride-suppressed promoter activity of the nuclear factor-kappa B (NF-κB)-luciferase reporter gene, suggesting that PPARγ may interfere with NF-κB transcriptional activity via coactivator competition.