activation of NF-κB and AP-1 is acting to transrepress PPARδ [35]. Furthermore, LPS-induced Cox-2 expression in rat primary astrocytes may be modulated, in part, by PPARδ. In particular, rosiglitazone, a PPARγ agonist, increased PPARδ expression in cortical astrocytes and led to increased Cox-2 expression. On the other hand, GW7647, a PPARα agonist, reduced PPARδ levels and decreased LPS-induced Cox-2 expression [67]. These results are surprising given that studies largely focus on the antioxidant and anti-inflammatory properties of PPARs.
