Baicalin attenuates Alzheimer-like pathological changes and memory deficits induced by amyloid β1–42 protein
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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) 1–42 protein-induced Alzheimer’s disease (AD). Mice received a bilateral injection of Aβ1–42 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 Aβ1–42 protein. These results suggest that baicalin ameliorated Aβ1–42 protein-related pathology and cognitive dysfunction via its anti-neuroinflammatory activity, and may be a potential candidate for the treatment of AD.
KeywordsAlzheimer’s disease Baicalin Neuroinflammation Memory Glial activation
This work was supported by the National Nature Scientific Fund of China (81,271,392, 81,301,050) and the Fund of Logistics University of Chinese People’s Armed Police Forces (WHTD201306-1). The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
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