Skip to main content
Figure 1 | Journal of Neuroinflammation

Figure 1

From: Telmisartan directly ameliorates the neuronal inflammatory response to IL-1β partly through the JNK/c-Jun and NADPH oxidase pathways

Figure 1

Telmisartan inhibits interleukin-1 beta (IL-1β)-induced cyclooxygenase-2 (COX-2) mRNA and protein expression and prostaglandin E 2 (PGE 2 ) release in SK-N-SH neuroblasts (A,B) IL-1β dose-dependently and time-dependently induces COX-2 mRNA expression in SK-N-SH neuroblasts. The cells were incubated with (A) the indicated concentrations of IL-1β for 3 hours, or with (B) 10 ng/ml IL-1β at indicated time intervals to determine COX-2 mRNA expression. Results are expressed as fold change relative to vehicle-treated group (Veh). (C) Telmisartan, candesartan, and losartan reduced IL-1β induced COX-2 mRNA expression with similar potency. The cells were pretreated with 10 μmol/l telmisartan (Telm), candesartan (Cand), or losartan (Los) for 2 hours before exposure for 3 hours to 10 ng/ml IL-1β. Results are expressed as the percentage of IL-1β. (D) Telmisartan was the most effective of AT1 receptor blockers at reducing the IL-1β-induced PGE2 release. Cells were pretreated with indicated concentrations of Telm, Cand, or Los for 2 hours before exposure for 24 hours to 10 ng/ml IL-1β to determine cumulative PGE2 release. Results are expressed as the percentage of IL-1β. (E,F) Telmisartan dose-dependently reduced IL-1β-induced COX-2 mRNA and protein expression. The cells were pretreated with indicated concentrations of Telm for 2 hours, then incubated with 10 ng/ml IL-1β for (E) 3 hours to determine COX-2 mRNA expression, or (F) 24 hours to determine COX-2 protein expression. The picture is a representative western blot. All results are means ± SEM from at least three independent experiments. * P < 0.05, ** P < 0.01, *** P < 0.001 vs. IL-1β; # P < 0.05, ### P < 0.001 vs. Veh; $$$ P < 0.001 vs. IL-1β + 10 μmol Telm.

Back to article page