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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.


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Curcumin reduces hippocampal neuron apoptosis and JNK-3 phosphorylation in rats with Aβ-induced Alzheimer’s disease: protecting spatial learning and memory

Show Author's information Yun-liang Wang1,2,*Jin-feng Li1,*Yu-tong Wang3Chun-yang Xu2Lin-lin Hua2Xiao-peng Yang2Shuang Geng1Shan-shan Wang1Zhen Wang1Hong-lei Yin1( )
Neurology Department, 148th Hospital, Zibo, Shandong,
Neurology Department, Second Affiliated Hospital of Zhengzhou University, Zhengzhou,
Public 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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Published: 21 June 2017
Issue date: December 2017

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© 2017 The Author(s).

Acknowledgements

This work was supported by the National Natural Science Foundation of China under the grant number 30770762. Our sincere thanks to Dr Ming-yao Du and Jing Zhao, who made great contributions to the behavioral tests.

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