Figure 3
Expression levels of GSK, ERK and JNK in the APP/PS1 mouse brain 20 weeks after STZ treatment. (A) Immunoblot analyses showing the protein levels of GSK-3α and GSK-3β in transgenic mouse brain. β-actin was used as a loading control. (B) A marked reduction in p-GSK3α level was detected in STZ-treated mouse brain. Also the ratio of p-GSK3α/GSK3α was significantly reduced after STZ treatment. (C) Insulin deficiency reduced GSK3β phosphorylation, and resulted in a reduced ratio of p-GSK3β/GSK3β in STZ-induced diabetic mouse brain. (D) Immunoblot analyses showing the expression levels of ERK in transgenic mouse brain. β-actin was used as a loading control. (E) Administration of STZ resulted in a reduced ratio of p-ERK/ERK, but this was not statistically significant compared with the vehicle control. (F) Immunoblot analyses showing the expression levels of JNK in transgenic mouse brain. β-actin was used as a loading control. (G) STZ treatment increased JNK1 phosphorylation and the ratio of p-JNK1/JNK1 was significantly increased in STZ-induced diabetic mouse brain. (H) The expression levels of p-JNK2 and the ratio of p-JNK2/JNK2 were significantly increased in STZ-induced diabetic mouse brain. *p < 0.05, **p < 0.01 (n = 7).