| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
|
|---|
| Outline of Final Research Achievements |
Prostaglandin E2 (PGE2) potentiated interferon-γ (IFN-γ)-induced nitric oxide production in cultured rat microglia. Instead of PGE2, EP2 agonist, butaprost, enhanced IFN-γ-induced nitric oxide production, and EP2 antagonist, TG4-155, reversed the effect of PGE2 on IFN-γ-induced nitric oxide production. These results suggest that PGE2 activates EP2 receptor, which potentiates IFN-γ-induced nitric oxide production. PGE2 is also reported to reduce phagocytosis of amyloid-β in microglia, indicating that Alzheimer's disease is exacerbated by PGE2 signaling. It is, therefore, suggested that the inhibition of PGE2 signaling is a potential strategy for the treatment of Alzheimer's disease.
|
