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Free Radic Biol Med. 2019 Jan;130:458-470. doi: 10.1016/j.freeradbiomed.2018.11.014. Epub 2018 Nov 15.

Using the synthesized peptide HAYED (5) to protect the brain against iron catalyzed radical attack in a naturally senescence Kunming mouse model.

Author information

1
Guangxi Key Laboratory of Brain and Cognitive Neuroscience, Guilin Medical University, Guilin, GX 541199, China; Medical School of Taizhou University, Taizhou, ZJ 318000, China; Biochemistry Department, Purdue University, West Lafayette, IN 47906, USA. Electronic address: zouzy@glmc.edu.cn.
2
Genetic Department of Nanjing Medical University, Nanjing, JS 210000, China.
3
Medical School of Taizhou University, Taizhou, ZJ 318000, China.
4
Clinical Laboratory of Affiliated Hospital of Taizhou University, Taizhou, ZJ 318000, China. Electronic address: zhouy5077@tzzxyy.com.
5
Medical Image Center of Affiliated Hospital of Taizhou University, Taizhou, ZJ 318000, China. Electronic address: wangzx@tzzxyy.com.
6
Guangxi Key Laboratory of Brain and Cognitive Neuroscience, Guilin Medical University, Guilin, GX 541199, China.
7
Shangli Teacher Training School, Pingxiang, JX 337009, China.

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disease of the brain. It cannot be cured currently, and those suffering from AD place a great burden on their caregivers and society. AD is characterized by high levels of iron ions in the brain, which catalyze radicals that damage the neurons. Knowing that the Aβ42 peptide precipitates iron by binding iron ions at amino acid residues D1, E3, H11, H13, and H14, we synthesized a 5-repeat (HAYED) sequence peptide. By treating iron-stressed SH-SY5Y cells with it and injecting it into the cerebrospinal fluid (CSF) of naturally senescence Kunming mouse, which displaying AD-similar symptoms such as learning and memory dysfunction, neuron degeneration and high level of iron in brain, we found that HAYED (5) decreased the iron and radical levels in the cell culture medium and in the CSF. Specially, the synthesized peptide prevented cell and brain damage. Furthermore, functional magnetic resonance imaging (fMRI), Morris water maze and passive avoidance tests demonstrated that the peptide ameliorated brain blood-oxygen metabolism and slowed cognitive loss in the experimental senescence mice, and clinical and blood tests showed that HAYED (5) was innoxious to the kidney, the liver and blood and offset the AD-associated inflammation and anemia.

KEYWORDS:

Alzheimer's disease; Amyloid β peptide; Free iron ions; HAYED (5) peptide; Radicals; Senescence

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