Fig. 5
TNAP pharmacological inhibition leads to increased levels of OPN, P2X7, and LRP1 in APP/PS1+/−mice. (A) Representative immunoblot using an antibody recognizing cleaved and full-length OPN in homogenates from the hippocampus of WT, WT treated with Levamisole (WT Leva), APP/PS1+/−, and APP/PS1+/− treated with Levamisole (APP/PS1+/− Leva). (B and C) Quantification of the ratio between cleaved OPN and full-length OPN (K) and total OPN (L) protein levels in the hippocampus of WT (n = 12), WT Leva (n = 6), APP/PS1+/− Leva (n = 8) and APP/PS1+/− (n = 11) mice. (D) Representative immunoblot of LRP1, IL-1β, P2X7, NLRP3, and MMP9 in homogenates from the hippocampus of WT, Levamisole-treated WT (WT Leva), untreated APP/PS1+/−, and Levamisole-treated APP/PS1+/− (APP/PS1+/− Leva) mice. Quantification of P2X7 (E), IL-1β (F), NLRP3 (G), LRP1 (H), and MMP9 (J) protein levels in the hippocampus of WT (n = 10), WT Leva (n = 6), APP/PS1+/− Leva (n = 8) and APP/PS1+/− (n = 11) mice. Levels of α-tubulin were used as loading control for normalization purposes. Data are given as a percentage relative to WT mice #P ≤ 0,08, * P ≤ 0.05 or ** P ≤ 0.01, using a one-way ANOVA followed by Tukey’s post hoc test. I. Graphs show the Aβ1−40 levels in serum samples from APP/PS1+/− (n = 8), the same that were previously shown in Fig. 3O, and APP/PS1+/− Leva (n = 4) mice. Serum samples were analyzed via Aβ1−40-detecting ELISA. Data in box plots represent the distribution of values per group (median, IQR, maximum, and minimum values)