Fig. 6
From: MH84 improves mitochondrial dysfunction in a mouse model of early Alzheimer’s disease
Analysis of mitochondrial respiration of isolated brain mitochondria (a) performed using an Oxygraph-2 k system. Animals belonged to three different study groups (wild-type(control), Thy-1 AβPPSL (control), and treatment group Thy-1 AβPPSL (MH84)). To analyze mitochondrial function different substrates, uncouplers and inhibitors were added; for details please refer to Methods. Data represent means ± SEM from 10 experiments; two-way ANOVA with Bonferroni post test (*p < 0.05 against wild-type(control); +++p < 0.001 against Thy-1 AβPPSL (control)). Basal mitochondrial membrane potential (MMP; R123 fluorescence) (b) and ATP levels (c) of mitochondria measured in dissociated brain cells. MMP determined using R123 as fluorescence dye. ATP levels determined using a bioluminescence assay. Data represent means ± SEM. N = 11 (six females, five males); one-way ANOVA with Tukey’s multiple comparison post test (*p < 0.05 against wild-type(control); +p < 0.05, ++p < 0.01 against Thy-1 AβPPSL (control)). CI complex I (NADH reductase, CII complex II (succinate dehydrogenase), CIV complex IV (cytochrome-c oxidase), ETS electron transfer system, AβPP beta-amyloid precursor protein