Fig. 4

Chronic oral DMF administration suppresses the expression of neuroinflammatory molecules in the glial cells of App-KI mice. A Schematic overview of gene expression analysis of microglia and astrocytes isolated from the cerebral cortices of DMF- or vehicle-administered WT and App-KI mice using MACS. B Expression levels of mRNAs in isolated microglia from DMF- or vehicle (Veh) -administered WT and App-KI mice determined by quantitative PCR. Relative expression levels of Nrf2 (Nfe2l2) and its downstream molecule Osgin1, complements and their receptors (C1qα and C3αr), DAM marker (Cd11c), inflammation factors (Tnf and Il1a), and inflammation regulator (Socs3) are plotted as means ± SEM. [Veh-WT (n = 7–12), DMF-WT (n = 6–12), Veh-App-KI (n = 7–12), and DMF-App-KI (n = 8–12)]. *p < 0.05 and **p < 0.01 (two-way ANOVA). C Expression levels of mRNAs in isolated astrocytes from DMF- or vehicle (Veh)-administered WT and App-KI mice determined by quantitative PCR. Relative expression levels of Nrf2 (Nfe2l2) and its downstream molecule Osgin1, and A1 astrocyte marker, (H2d), a complement (C3), inflammation regulators (Socs3 and Stat3), and astroglial activation marker (Gfap) are represented as means ± SEM. [Veh-WT (n = 6–11), DMF-WT (n = 6–11), Veh-App-KI (n = 5–9), and DMF-App-KI (n = 7–12)]. *p < 0.05 and **p < 0.01 (two-way ANOVA)