Figure 4. The key role of COX-2 in regulating the expression of APH-1α/1β and PS1 during the course of AD progression. (A) Three-month-old COX-2 Tg mice were injected (i.c.v) with NS398 (1 μg/5 μl) for 48 h (n=12). (B) In select experiments, n2a cells were transfected with COX-2 cDNA constructs in the absence or presence of NS398 treatment (10 μM). (C) In separate experiments, C57BL/6 mice were injected (i.c.v) with Aβ (500 ng/5 μl) in the absence or presence of NS398 (1 μg/5 μl) for 48 h. (D) In distinct experiments, n2a cells were treated with Aβ oligomers (1 μM) in the absence or presence of NS398 (10 μM) for 48 h. The mRNA and protein levels of APH-1α/1β and PS1 were determined by qRT-PCR and western blots, respectively. GAPDH and β-actin served as internal controls. The data represent the means±S.E. of all the experiments. *p<0.05; **p<0.01 compared with C57BL/6, vector-transfected or vehicle-treated n2a controls. # p<0.05 with respect to COX-2 Tg mice or Aβ-treated mice alone.