| Summary: | Yun-liang Wang,1,2,* Jin-feng Li,1,* Yu-tong Wang,3 Chun-yang Xu,2 Lin-lin Hua,2 Xiao-peng Yang,2 Shuang Geng,1 Shan-shan Wang,1 Zhen Wang,1 Hong-lei Yin1 1Neurology Department, 148th Hospital, Zibo, Shandong, 2Neurology Department, Second Affiliated Hospital of Zhengzhou University, Zhengzhou, 3Public Health Department, Henan University School of Medicine, Kaifeng, Henan, People’s Republic of China *These authors contributed equally to this work 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 Aβ1–40 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. Aβ1–40 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
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