Format

Send to

Choose Destination
Am J Alzheimers Dis Other Demen. 2015 Mar;30(2):183-91. doi: 10.1177/1533317514542645. Epub 2014 Jul 13.

Sulforaphane ameliorates neurobehavioral deficits and protects the brain from amyloid β deposits and peroxidation in mice with Alzheimer-like lesions.

Author information

1
Department of Nutrition and Food Hygiene, School of Public Health, China Medical University, Shenyang 110001, China.
2
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 the elderly individuals and its effective therapies are still unavailable. This study was designed to investigate the neuroprotection of sulforaphane (SFN) in AD-lesion mice induced by combined administration of d-galactose and aluminium. Results showed that SFN ameliorated spatial cognitive impairment and locomotor activity decrease in Morris water maze and open field test, respectively. And attenuated numbers of amyloid β (Aβ) plaques in both hippocampus and cerebral cortex of AD-lesion mice were detected by immunohistochemistry. According to spectrophotometry and quantitative reverse-transcriptase polymerase chain reaction results, a significant increase in carbonyl group level and obvious decreases in both activity and messenger RNA expression of glutathione peroxidase were found in brain of AD-lesion mice compared with control, but not in SFN-treated AD-lesion mice. In conclusion, SFN ameliorates neurobehavioral deficits and protects the brain from Aβ deposits and peroxidation in mice with Alzheimer-like lesions, suggesting SFN is likely a potential phytochemical to be used in AD therapeutics.

KEYWORDS:

Alzheimer’s disease; amyloid β; neurobehavior; oxidative stress; phytochemical; sulforaphane

PMID:
25024455
DOI:
10.1177/1533317514542645
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Atypon
Loading ...
Support Center