The nuclear factor-kappa B (NF-κB) pathway is not involved in the neuroprotective effect of telmisartan in SK-N-SH neuroblasts. (A) Telmisartan does not prevent time-dependent IκB-α protein degradation in cells in response to interleukin-1 beta (IL-1β). Cells were pretreated for 2 hours with 10 μmol/l telmisartan (Telm) before exposure to 10 ng/ml IL-1β for the indicated time intervals. IκB-α protein levels were determined in whole-cell extracts, and normalized to β-actin. (B) Neither telmisartan nor diphenyleneiodonium (DPI) modified IL-1β-induced expression of IκB-α mRNA. The cells were pretreated for 2 hours with 10 μmol/l Telm or 5 μmol/l DPI before exposure for 3 hours to 10 ng/ml IL-1β to determine IκB-α mRNA expression. (C) Neither telmisartan nor DPI affected IL-1β-induced nuclear translocation of the NF-κB p65 subunit. The cells were pretreated for 2 hours with 10 μmol/l Telm or 5 μmol/l DPI before exposure for 30 minutes to 10 ng/ml IL-1β. The NF-κB p65 subunit protein was determined in nuclear extracts and normalized to the level of the nuclear protein histone H4. Representative western blots are shown below the corresponding bar graphs. Results are presented as means ± SEM from three independent experiments. # P < 0.05, ### P < 0.001 vs. Veh.