Abstract: Amyloid-β peptide (Aβ) toxicity in Alzheimer’s disease (AD) is associated with the c-Jun N-terminal kinase (JNK) signaling pathway. Curcumin may prevent Aβ fiber formation, slowing AD progression. A model of AD was established in 32 Sprague Dawley rats by injection of 10 μg Aβ_1–40 into the right hippocampus. Saline was used in sham control (n=16). Sixteen AD model rats received 300 mg/kg curcumin and another 16 received saline daily for 7 days. Spatial learning and memory were assessed using a Morris water maze. Hippocampus neuron apoptosis and hippocampal levels of JNK-3 and p-JNK-3 were assessed by terminal deoxynucleotidyl transferase dUTP nick end labeling, reverse transcription-polymerase chain reaction and Western blotting. Aβ_1–40 injection induced slower spatial learning, memory deficit, neuronal apoptosis and increased JNK-3 expression and phosphorylation (all P <0.05). Curcumin relieved spatial learning and memory deficits, hippocampus neuronal apoptosis, and reduced JNK-3 and p-JNK-3 levels (all P <0.05). In conclusion, curcumin may inhibit JNK-3 phosphorylation to protect against hippocampal neuron apoptosis after Aβ injection.
Keywords: Alzheimer’s disease, curcumin, apoptosis, JNK-3, phosphorylation