Fig. 4

PGC-1α inhibits NF-κB pathway induced by Aβ1–42 in N2a cells. N2a cells transfected with an empty vector or PGC-1α overexpression plasmid were treated with or without Aβ1–42 (25 μM) for 6 h. a Cytoplasmic extracts, nuclear extracts and whole cell lysates were prepared and subjected to Western blot analysis for NF-κB p65, Lamin B1, p-IκBα, IκBα, and β-actin was used as loading control. The levels of b Cytoplasmic NF-κB p65, c nuclear NF-κB p65, d p-IκBα, and e IκBα were quantified by densitometry. Results shown are representative as mean ± SEM (two-way ANOVA with Bonferroni post-tests) for three independent experiments. ***p < 0.001 compared to control group