A study of microglial function to cure Alzheimer disease

PGE2降低培养大鼠小胶质细胞活力。细胞活力的降低是由于细胞凋亡。两种PGE2受体激动剂，一种是EP2受体激动剂丁前列腺素，一种是EP4受体激动剂PGE1醇，也能诱导小胶质细胞凋亡。然而，EP1 - EP4拮抗剂不能逆转pge2降低的细胞活力。另一方面，GSK-3抑制剂SB216763逆转了pge2降低的细胞活力。此外，PGE2可降低磷酸化GSK-3水平。PGE2诱导小胶质细胞凋亡，而GSK-3参与了这种凋亡。

PGE2 reduced cell viability in cultured rat microglia. This reduction in cell viability was due to apoptosis. Microglial apoptosis was also induced by two PGE2 receptor agonists, an EP2 agonist butaprost and an EP4 agonist PGE1 alcohol. However, PGE2-reduced cell viability was not reversed by EP1 - EP4 antagonists. On the other hand, PGE2-reduced cell viability was reversed by GSK-3 inhibitor SB216763. In addition, phsophorylated GSK-3 level was reduced by PGE2. There data suggest that PGE2 induces apoptosis in microglia, and this apoptosis is involved in GSK-3.