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. 2014 Mar 13;13(4):605–615. doi: 10.1111/acel.12209

Figure 3.

Figure 3

IL-1β induces mRNA and protein expression of COX-2, which in turn up-regulates BACE-1 expression and activates of the PI3-K/AKT, PKA/CREB signaling pathways in a HSP70-, PGE2- or forskolin-dependent manner in human- or mouse-derived neuron cells. Human neuroblastoma SH-SY5Y (A, C) and mouse neuroblastoma n2a cells (B, D) were treated with IL-1β (100 ng mL−1) or VER155008 (10 μm) for 48 h. In selected experiments, SH-SY5Y cells were treated with NS398 (50 μm) in the absence or presence of IL-1β (100 ng mL−1) for 48 h (E). In separate experiments, SH-SY5Y cells were treated with PGE2 (10 μm) or forskolin (10 μm) for 48 h (F). The total COX-2, BACE-1 (A, B upper panel) and phosphorylated AKT, CREB, NF-κB levels (A, B, E, F upper panel) were detected by immunoblotting using specific Abs. The equal lane loading is demonstrated by the similar intensities of the total AKT, CREB, NF-κB and β-actin. The COX-2, BACE-1 mRNA levels (A, B, E, F lower panel) were determined by qRT–PCR, and the total amounts of GAPDH served as internal controls. The formation of PGE2 and cAMP (C, D) was determined using PGE2 and cAMP enzyme immunoassay kits, respectively. The data represent the means ± SE of three independent experiments. *P < 0.05 with respect to the vehicle-treated control. #P < 0.05 compared to treatments with IL-1β, PGE2, or forskolin alone.