Angelica tenuissima Nakai Ameliorates Cognitive Impairment and Promotes Neurogenesis in Mouse Model of Alzheimer’s Disease

Minji Choi; Younghyurk Lee; Seung-Hun Cho

doi:10.1007/s11655-017-2812-2

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Angelica tenuissima Nakai Ameliorates Cognitive Impairment and Promotes Neurogenesis in Mouse Model of Alzheimer’s Disease

Updated：2021-08-27

- Angelica tenuissima Nakai Ameliorates Cognitive Impairment and Promotes Neurogenesis in Mouse Model of Alzheimer’s Disease
- Chinese Journal of Integrative Medicine Vol. 24, Issue 5, Pages: 378-384(2018)
- Affiliations：
  
  Department of Psychiatry, Hospital of Korean Medicine, Kyung Hee University Medical Center, Seoul, South Korea
- Author bio：
- Funds：
  
  Supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT & Future Planning (No. NRF-2013R1A1A1063477)
- DOI：10.1007/s11655-017-2812-2
  CLC：
- Published：2018，
  
  Published Online：3 June 2017，
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Choi, M., Lee, Y. & Cho, SH. Angelica tenuissima Nakai Ameliorates Cognitive Impairment and Promotes Neurogenesis in Mouse Model of Alzheimer’s Disease., Chin. J. Integr. Med. 24, 378–384 (2018). https://doi.org/10.1007/s11655-017-2812-2

Minji Choi, Younghyurk Lee, Seung-Hun Cho. Angelica tenuissima Nakai Ameliorates Cognitive Impairment and Promotes Neurogenesis in Mouse Model of Alzheimer’s Disease. [J]. Chinese Journal of Integrative Medicine 24(5):378-384(2018)
Choi, M., Lee, Y. & Cho, SH. Angelica tenuissima Nakai Ameliorates Cognitive Impairment and Promotes Neurogenesis in Mouse Model of Alzheimer’s Disease., Chin. J. Integr. Med. 24, 378–384 (2018). https://doi.org/10.1007/s11655-017-2812-2 DOI：

Minji Choi, Younghyurk Lee, Seung-Hun Cho. Angelica tenuissima Nakai Ameliorates Cognitive Impairment and Promotes Neurogenesis in Mouse Model of Alzheimer’s Disease. [J]. Chinese Journal of Integrative Medicine 24(5):378-384(2018) DOI： 10.1007/s11655-017-2812-2.

摘要

To research Angelica tenuissima Nakai (ATN) for use in novel Alzheimer’s disease (AD) therapeutics. 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 fifield 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 [neuronspecific 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. 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. KH032 attenuated cognitive defificits in the Aβ1-42-infused mice by increasing BDNF expression and ERK1/2 and CREB phosphorylation and inhibiting neuronal loss and neuroinflflammatory response

suggesting that KH032 has therapeutic potential in neurodegenerative disorders such as AD.

Abstract

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 fifield 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 [neuronspecific 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. 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

suggesting that KH032 has therapeutic potential in neurodegenerative disorders such as AD.

关键词

Alzheimer’s diseaseAngelica tenuissima Nakaibeta amyloidcognitive impairmentneurogenesis

Keywords

Alzheimer’s diseaseAngelica tenuissima Nakaibeta amyloidcognitive impairmentneurogenesis

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