Figure 3
From: Glycation exacerbates the neuronal toxicity of β-amyloid

Activation of GSK-3β is involved in the exacerbated neurotoxicity of Aβ-AGE in hippocampal neurons. (a–c) Hippocampal neurons cultured 8 DIV were treated with Aβ or Aβ-AGE for 24 h, then the level of phosphorylated GSK-3β at Ser9 (inactive form) was measured by western blot (a and b) and immunofluorescence (c). (d–k) Hippocampal neurons cultured 8 DIV were pre-incubated with or without LiCl (inhibitor of GSK-3) before treatment of Aβ or Aβ-AGE for 24 h. Then the neuron viability (d), the apoptotic rate (e), levels of the phosphorylated tau (f and g), synaptic proteins (h and i), and Akt (j and k) were measured. The level of phosphorylated GSK-3β, phosphorylated tau, synaptic proteins, and phosphorylated Akt was normalized, respectively, to GSK-3β, Tau5, DM1A, and Akt. Li: LiCl. n=3, *P<0.01 versus Aβ group. #P<0.01 versus Aβ-AGE group. Scale bar in c, 50 μm