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Cyclooxygenase-2 (COX-2) has been recently identified as being involved in the pathogenesis of Alzheimer’s disease (AD). However, the role of an important COX-2 metabolic product, prostaglandin (PG) I 2 , in AD development remains unknown. Using mouse-derived astrocytes as well as APP/PS1 transgenic mice as model systems, we firstly elucidated the mechanisms of interferon γ (IFNγ) regulation by PGE 2  and PGI 2 . Specifically, PGE 2  accumulation in astrocytes activated the ERK1/2 and NF-κB signaling pathways by phosphorylation, which resulted in IFNγ expression. In contrast, the administration of PGI 2  attenuated the effects of PGE 2  on stimulating the production of IFNγ  via  inhibiting the translocation of NF-κB from the cytosol to the nucleus. Due to these observations, we further studied these prostaglandins and found that both PGE 2  and PGI 2  increased Aβ 1–42  levels. In detail, PGE 2  induced IFNγ expression in an Aβ 1–42 -dependent manner, whereas PGI 2 -induced Aβ 1–42  production did not alleviate cells from IFNγ inhibition by PGI 2  treatment. More importantly, our data also revealed that not only Aβ 1–42  oligomer but also fibrillar have the ability to induce the expression of IFNγ via stimulation of NF-κB nuclear translocation in astrocytes of APP/PS1 mice. The production of IFNγ finally accelerated the deposition of Aβ 1–42  in β-amyloid plaques.

Prostaglandin I2 Attenuates Prostaglandin E2-Stimulated Expression of Interferon γ in a β-Amyloid Protein- and NF-κB-Dependent Mechanism