Figure 3
From: Combining two repurposed drugs as a promising approach for Alzheimer's disease therapy
ABC protects Aβ1–42-intoxicated neuronal cells from apoptosis by normalising several induced alterations.
(a) ABC reduced oxidative stress as assessed by MetO staining. Neurons with MetO (in red) overlapping with MAP2 (in green) were counted and results were expressed as percentage of untreated control. (b) Normalisation by ABC of cell-released glutamate quantified in the medium of Aβ-intoxicated neurons. (c) Preservation by ABC of phosphorylated tau protein (pTauSer212/Thr214, green) quantified in Aβ-intoxicated neurons (red). (d) Synaptic integrity was preserved following ABC treatment, as assessed by the co-localisation of pre-synaptic synaptophysin (red) and post-synaptic PSD95 (green) proteins. Scale bars: 60 μm. Values are mean ± s.e.m. ***P < 0.001 versus Aβ; ANOVA with Dunnett's test. ABC was composed of 0.32 nM ACP and 80 nM BCL. BDNF was used as positive control (50 ng mL−1). MetO: Oxidised methionines; PSD95: Post-synaptic density protein 95. Blue: Hoechst.
