Figure 5.

COX-2 mediated the reciprocal regulation of Aβ and IL-1β between glial and neuron cells; this reciprocal regulation in turn potentially contributes to the progression of Alzheimer’s disease (AD). A172 cells were incubated in conditioned medium, which was collected from neo or sw cells in the absence or presence of Aβ antibody (0.5 μg mL⁻¹) (A). In selected experiments, the neo or sw cells were treated with conditioned medium, which was collected from A172 cells in the absence or presence of IL-1β antibody (1 μg mL⁻¹) (B). Similar experiments were performed between C6 and n2a cells (C, D). The mRNA and protein levels of COX-2 (A, C), IL-1β (A, C) and BACE-1 (B, D) were determined by qRT–PCR and Western blots, respectively. The total amounts of GAPDH and β-actin served as internal controls for the qRT–PCR and Western blots, respectively. The data represent the means ± SE of three independent experiments. *P < 0.05 with respect to the untreated control. #P < 0.05 compared to treatment with just the conditioned medium.