期刊
EUROPEAN JOURNAL OF PHARMACOLOGY
卷 621, 期 1-3, 页码 38-45出版社
ELSEVIER
DOI: 10.1016/j.ejphar.2009.08.036
关键词
L-3-n-butylphthalide (L-NBP); Amyloid-beta; Learning and memory deficits; Alzheimer's disease; Tau protein phosphorylation
资金
- National 973 Fundamental Project of China [2004CB518906]
- Natural Science Foundation of Beijing [7093125]
- Chinese Herbal Medicine
- Ministry of Education
Alzheimer's disease is the most common form of dementia. Amyloid-P protein is considered as a key factor of pathogenesis of Alzheimer's disease. L-3-n-butylphthalide (L-NBP), an anti-cerebral ischemia drug, has been shown to have therapeutic effects in vascular dementia animal models. In the present study, we investigated the potential of L-NBP to protect against cognitive impairment, oxidative damage and neuropathological changes induced by intracerebroventricular infusion of amyloid-beta peptide in rats. Daily treatments of 10 and 30 mg/kg L-NBP significantly improved spatial learning deficits and attenuated working memory deficits in Morris water maze task. L-NBP partially reversed the reduction of glutathione peroxidase activities and decreased malondialdehyde levels in the cortex and hippocampus. Furthermore, L-NBP markedly inhibited amyloid-beta-induced neuronal apoptosis, possibly by blocking caspase-3 activation. In addition, L-NBP reduced activation of glycogen synthase kinase-3 beta and tau protein phosphorylation. Our results demonstrate that L-NBP protects against amyloid-beta-induced neurodegeneration and cognitive decline in a rat model, suggesting that it may have potential as a therapy for Alzheimer's disease. (C) 2009 Published by Elsevier B.V.
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