Figure 2.

Carprofen affects the expression levels of key Alzheimer-like biomarkers involved in Aβ aggregation. (a, b) Dot blots and densitometry of the cortical and hippocampal regions to quantify the total soluble Aβ and oligomer concentrations by utilizing anti-Aβ 6E10 antibody and anti-oligomer A11 antibody, respectively. (c, d) The aggregated Aβ levels of vehicle- and carprofen-treated groups in both the cortex and hippocampus after ELISA. (e–g) Western blot and densitometry of Alzheimer-related biomarkers in (f) cortex and (g) hippocampus brain lysates. The densitometry data analyzed the levels of GFAP, Iba-1, PSD95, synaptophysin, and phosphorylated tau expressions. The original dot blots and full-membrane results with their respective β-actins are presented in Supplementary Fig. S3. All data represent the mean ± SEM and the statistical analyses were performed by one-way analysis of variance excluding ELISA data using two-tailed unpaired t-test with the comparison to the vehicle-treated 5XFAD mice group (Veh, black) (*P < 0.05, **P < 0.01, ***P < 0.001, other comparisons not significant). Wt, wild-type; Veh, vehicle; Car, carprofen; GFAP, glial fibrillary acidic protein; Iba-1, ionized calcium-binding adaptor molecule 1; PSD95, post-synaptic density protein 95; Syn, synaptophysin; AT8, phosphorylated tau (S202, T205).