Fig. 4
Amyloid β (Aβ)-induced reduction on mitochondrial biogenesis is restored after S14 treatment. a Upper panel shows representative Western blot bands, and the lower panel shows increased peroxisome proliferator-activated receptor γ co-activator α (PGC-1α) expression in the hippocampus of S14-treated APP/PS1 mice compared with the vehicle (Veh)-treated group (n = 5–7 mice per group; *p < 0.05). b Representative immunoblots (upper panels) and protein level quantification detected by Western blot (lower panel) showing a significant reduction in the expression of complex V β subunit (CxVβ) in the hippocampus of S14-treated APP/PS1 mice compared with the vehicle-treated group (n = 5–7 mice per group; *p < 0.05). When transgenic mice were treated with S14, CxVβ levels were recovered. Data are expressed as mean ± SEM. c Mitochondrial mass was measured in live cells using the human neuroblastome SH-SY5Y cell line simultaneously exposed to 1 μM oligomeric Aβ42 for 24 h and evaluated by confocal imaging. d Imaging analysis revealed a reduced amount of mitochondrial volume from the whole cell volume in Aβ42-exposed cells compared to untreated cells. Treatment with 15 μM S14 on Aβ42-exposed cells obliterated this effect, showing no changes on the unexposed cells. Data are expressed as mean ± SEM; n = 4; *p < 0.05; **p < 0.01. e,f Representative immunoblots (upper panel) and quantification of the measures detected by Western blot (lower panel) showing a significant reduction in the CxVβ levels (e) and PGC-1α (f) in SH-SY5Y cells exposed to 1 μM oligomeric Aβ42. When cells were co-treated with 15 μM S14, CxVβ (e) and PGC-1α (f) expression were recovered. Data are expressed as mean ± SEM; n = 4; **p < 0.01; ***p < 0.001; ****p < 0.0001. Statistical significance was assessed by two-way ANOVA followed by Fisher’s post-hoc test for multiple comparisons. wt wild-type