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Int J Mol Sci. 2014 Aug 18;15(8):14396-410. doi: 10.3390/ijms150814396.

Neuroprotective effects of sulforaphane on cholinergic neurons in mice with Alzheimer's disease-like lesions.

Author information

1
Department of Nutrition and Food Hygiene, School of Public Health, China Medical University, Shenyang 110001, China. z_zhangrui@163.com.
2
Department of Nutrition and Food Hygiene, School of Public Health, China Medical University, Shenyang 110001, China. zhangjz0107@163.com.
3
Department of Nutrition and Food Hygiene, School of Public Health, China Medical University, Shenyang 110001, China. fanglingduo@163.com.
4
Department of Nutrition and Food Hygiene, School of Public Health, China Medical University, Shenyang 110001, China. rabbitto89@163.com.
5
Department of Nutrition and Food Hygiene, School of Public Health, China Medical University, Shenyang 110001, China. yuezhao2000@163.com.
6
Department of Clinical Nutrition, First Affiliated Hospital, China Medical University, Heping District, Shenyang 110001, China. shiwanying2019@gmail.com.
7
Department of Nutrition and Food Hygiene, School of Public Health, China Medical University, Shenyang 110001, China. anli@mail.cmu.edu.cn.

Abstract

Alzheimer's disease (AD) is a common neurodegenerative disease in elderly individuals, and effective therapies are unavailable. This study was designed to investigate the neuroprotective effects of sulforaphane (an activator of NF-E2-related factor 2) on mice with AD-like lesions induced by combined administration of aluminum and D-galactose. Step-down-type passive avoidance tests showed sulforaphane ameliorated cognitive impairment in AD-like mice. Immunohistochemistry results indicated sulforaphane attenuated cholinergic neuron loss in the medial septal and hippocampal CA1 regions in AD-like mice. However, spectrophotometry revealed no significant difference in acetylcholine level or the activity of choline acetyltransferase or acetylcholinesterase in the cerebral cortex among groups of control and AD-like mice with and without sulforaphane treatment. Sulforaphane significantly increased the numbers of 5-bromo-2'-deoxyuridine-positive neurons in the subventricular and subgranular zones in AD-like mice which were significantly augmented compared with controls. Atomic absorption spectrometry revealed significantly lower aluminum levels in the brains of sulforaphane-treated AD-like mice than in those that did not receive sulforaphane treatment. In conclusion, sulforaphane ameliorates neurobehavioral deficits by reducing cholinergic neuron loss in the brains of AD-like mice, and the mechanism may be associated with neurogenesis and aluminum load reduction. These findings suggest that phytochemical sulforaphane has potential application in AD therapeutics.

PMID:
25196440
PMCID:
PMC4159858
DOI:
10.3390/ijms150814396
[Indexed for MEDLINE]
Free PMC Article

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