Fig. 5
From: Astrocytic autophagy plasticity modulates Aβ clearance and cognitive function in Alzheimer’s disease
Inhibition of astrocytic autophagy function dysregulates mitochondrial membrane potential and elevates ROS in response to Aβ oligomer. a, Representative images of mitochondrial membrane potential (by MitoTracker staining) and mitochondrial reactive oxygen species (ROS) (by MitoSOX staining) in Aβ oligomer-treated human astrocyte culture with or without E/P. Scale bars (white): 10 μm. b, Quantification of MitoTracker and MitoSOX signals in Aβ oligomer-treated human astrocytes with or without E/P. A total of 20 cell counts, 5 cells/well, n = 4 wells. c, Representative TEM images presenting ultrastructural changes of mitochondria in Aβ oligomer- and/or CQ-treated astrocytes. Scale bars (black): 0.5 μm. d. Quantification of the mitochondria size from EM images among four groups: control, 34 mitochondria counts; CQ, 26 mitochondria counts; Aβ, 29 mitochondria counts; Aβ + CQ, 29 mitochondria counts. Measurement of mitochondria size in 100 µm2 of ROI. e, Amplex UltraRed assay for detecting H2O2 in Aβ oligomer- and/or CQ-treated astrocytes. Bar graphs represent mean ± SEM from 6 wells. f, DCF-DA assay for detecting ROS in Aβ oligomer-treated astrocytes with or without KDS2010 (KDS), a ROS scavenger and reversible MAO-B inhibitor. Bar graphs represent mean ± SEM from 6 wells (control), 8 wells (Aβ), and 8 wells (Aβ + KDS2010). Significantly different at *, p < 0.05; **, p < 0.01