Figure 6.

Aβ-infused TgSREBP-2 mice display enhanced oxidative stress and neuronal damage which is prevented by GSH ethyl ester (GSHee) coinfusion. WT and TgSREBP-2 mice were subjected to continuous infusion of vehicle or human Aβ1–42 solution (1.2 μg/d) for 28 d. n = 6–8 mice per group. A, Lipid peroxidation estimated as production of malondialdehyde (MDA). *p < 0.03. B, Representative immunoblotting showing presence of carbonyl proteins in WT and TgSREBP-2 (Tg) brains after infusion. C, Representative immunoblotting showing synaptophysin (Synapt.) protein levels after infusion. Densitometric values of the bands representing synaptophysin immunoreactivity were normalized with the values of the corresponding β-actin bands (O.D.: normalized optical density). D, Representative images of degenerated neurons in hippocampal regions by Fluoro-Jade B staining. Scale bar: 50 μm. E, Representative images of apoptotic cells in hippocampus by terminal deoxynucleotidyl transferase-mediated nick-end labeling. Scale bar: 25 μm. F, Lipid peroxidation in infused TgSREBP-2 brains estimated as malondialdehyde levels (MDA). *p < 0.01 (n = 6). G, TNF-α and IL-1β mRNA expression analyzed by real-time PCR from infused TgSREBP-2 brains. Relative values were normalized against 18 s expression. *p < 0.05, **p < 0.01 (n = 6). Values are mean ± SD; mean differences were compared by unpaired Student's t test.