Protective effects of astragalosides on dexamethasone and A尾_25-35 induced learning and memory impairments due to decrease amyloid precursor protein expression in 12-month male rats

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• 作者：Wei-Zu Li^a ; ^b ; ¹ ; Wang-Yang Wu^a ; ^b ; ¹ ; Da-Ke Huang^c ; Yan-Yan Yin^a ; ^b ; Hong-Wei Kan^d ; Xin Wang^e ; Yu-You Yao^a ; ^b ; Wei-Ping Li^a ; ^b ; ^{lwp19@126.com}
• 关键词：Dexamethasone ; A尾25&ndash ; 35 ; Memory and learning impairment ; APP ; Astragalosides
• 刊名：Food and Chemical Toxicology
• 出版年：2012
• 期刊代码：20_02786915
• 类别：pha
• 出版时间：June, 2012
• 卷：50
• 期：6
• 页码：1883-1890
• 文件大小：1857 K

摘要

Alzheimer鈥檚 disease (AD) is a chronic neurodegenerative disorder of the elderly characterized by learning and memory impairment. Stress level glucocorticoids (GCs) and 尾-amyloid (A尾) peptide deposition are found to be correlated with dementia progression in patients with AD. The astragalosides (AST) was extracted from traditional Chinese herb Astragalus membranaceous. In this study, 12 months male rats were treated with A尾_25-35 (10 渭g/rat, hippocampal CA1 injection) and dexamethasone (DEX, 1.5 mg/kg, ig) and AST (8, 16 and 32 mg/kg, ig) or ginsenoside Rg1 (Rg1, 5 mg/kg, ig) for 14 days. We investigated the protective effect of AST against DEX + A尾_25-35 injury in rats and its mechanisms of action. Our results indicate that DEX + A尾_25-35 can induce learning and memory impairments and increase APP and A尾_1-40 expression. AST (16, 32 mg/kg) or Rg1 (5 mg/kg) treatment significantly improve learning and memory, down-regulate the mRNA levels of APP and 尾-secretase, decrease expression of APP and A尾_1-40 in hippocampus. The results indicated that DEX might increase hippocampal vulnerability to A尾_25-35 and highlight the potential neuronal protection of AST.