Baicalin attenuates Alzheimer-like pathological changes and memory deficits induced by amyloid β1-2 protein
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- 作者：Chong Chen ; Xiaohong Li ; Peilong Gao ; Yue Tu ; Mingliang Zhao…
- 关键词：Alzheimer’s disease ; Baicalin ; Neuroinflammation ; Memory ; Glial activation
- 刊名：Metabolic Brain Disease
- 出版年：2015
- 出版时间：April 2015
- 年：2015
- 卷：30
- 期：2
- 页码：537-544
- 全文大小：843 KB
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文摘
Baicalin is one bioactive flavone with anti-inflammatory and neuroprotective activities. The neuroprotective effects of baicalin on pathological changes and behavioral deficits were explored in a mouse model of amyloid β (Aβ) 1-2 protein-induced Alzheimer’s disease (AD). Mice received a bilateral injection of Aβ1-2 protein into the hippocampus, then they were treated with baicalin (30, 50 and 100?mg/kg body weight, orally) or Tween 80. The therapeutic effects of baicalin were monitored by Morris water maze trial and probe test. Then mice were sacrificed for immunohistochemistry and western blot analysis. After a relatively short-term treatment of 14?days, 100?mg/kg of baicalin significantly ameliorated memory impairment in the Morris water maze test and probe test, and also attenuated glial cell activations and increase of TNF-α and IL-6 expressions induced by Aβ1-2 protein. These results suggest that baicalin ameliorated Aβ1-2 protein-related pathology and cognitive dysfunction via its anti-neuroinflammatory activity, and may be a potential candidate for the treatment of AD.