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| Angelica tenuissima Nakai Ameliorates Cognitive Impairment and Promotes Neurogenesis in Mouse Model of Alzheimer's Disease |
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| KeyWord:Alzheimer's disease, Angelica tenuissima Nakai, beta amyloid, cognitive impairment, neurogenesis |
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| Abstract: |
| Objective: To research Angelica tenuissima Nakai (ATN) for use in novel Alzheimer's disease (AD) therapeutics. Methods: The effect of a 30% ethanol extract of ATN (KH032) on AD-like cognitive impairment and neuropathological and neuroinflammatory changes induced by bilateral intracerebroventricular injections of β-amyloid (Aβ) peptide (Aβ1-42) was investigated. Male C57Bl/6 mice were randomly divided into 4 groups, 10 in each group. KH032-treated groups were administrated with a low or high dose of KH032 (50 and 200 mg/kg, respectively), intragastrically for 16 days; distilled water was applied in the sham and negative groups. Open field test, Y maze and Morris water maze test were used for behavior test and cognitive ability. In addition, the neuroprotective effects of KH032 in Aβ1-42-infused mice on the histopathological markers [neuron-specific nuclear protein (NeuN), Aβ1-42] of neurodegeneration were examined. The levels of glial fibrillary acidic protein (GFAP), NeuN, phosphorylation extracellular signal-regulated kinase (ERK)/ERK, brain-derived neurotrophic factor (BDNF), phosphorylation cAMP response element-binding (CREB)/CREB protein expression were measured by Western blot. Results: KH032 treatment ameliorated cognitive impairments, reduced the overexpression of Aβ1-42, and inhibited neuronal loss and neuroinflammatory response in the Aβ1-42-infused mice. Moreover, KH032 treatment enhanced BDNF expression levels in the hippocampus. Finally, KH032 treatment increased phosphorylation of ERK1/2 and CREB, vital for ERK-CREB signaling. Conclusions: KH032 attenuated cognitive deficits in the Aβ1-42-infused mice by increasing BDNF expression and ERK1/2 and CREB phosphorylation and inhibiting neuronal loss and neuroinflammatory response, suggesting that KH032 has therapeutic potential in neurodegenerative disorders such as AD. |
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