Peroxisome proliferator-activated receptor gamma (PPARγ) activation is not involved in the neuroprotective effect of telmisartan in SK-N-SH neuroblasts. (A,B) The PPARγ agonist pioglitazone inhibited interleukin-1 beta (IL-1β)-induced cyclooxygenase-2 (COX-2) gene expression and prostaglandin E2 (PGE2) release. The cells were pretreated for (A) 2 hours with 10 μmol/l pioglitazone (PGZ) before exposure for 3 hours to 10 ng/ml IL-1β to determine COX-2 mRNA expression or (B) with indicated concentrations of PGZ before exposure for 24 hours to 10 ng/ml IL-1β to determine cumulative PGE2 release. (C) Pioglitazone, but not telmisartan, induced gene expression of the PPARγ target genes ABCG1 and CD36. The cells were incubated for 3 hours with 10 μmol/l PGZ or 10 μmol/l Telm to determine gene expression of PPARγ and its target genes ABCG1 and CD36. Results are shown as fold change relative to the vehicle-treated group (Veh). (D,E) PPARγ antagonists did not change the inhibitory effect of telmisartan on IL-1β-induced COX-2 expression. The cells were pretreated for 1 hour with 1 μmol/l T0070907 (T007) or 20 μmol/l GW9662 (GW), followed by 10 μmol/l Telm for 2 hours before exposure for (D) 3 hours to 10 ng/ml IL-1β to determine COX-2 mRNA, or (E) 24 hours of IL-1β to determine COX-2 protein expression. The picture below is a representative western blot. All results are means ± SEM from at least three independent experiments. * P < 0.05, *** P < 0.001 vs. IL-1β; # P < 0.05, ### P < 0.001 vs. Veh.