Angelica tenuissima Nakai Ameliorates Cognitive Impairment and Promotes Neurogenesis in Mouse Model of Alzheimer's Disease.
- Author:
Minji CHOI
1
;
Younghyurk LEE
1
;
Seung-Hun CHO
2
Author Information
- Publication Type:Journal Article
- Keywords: Alzheimer’s disease; Angelica tenuissima Nakai; beta amyloid; cognitive impairment; neurogenesis
- MeSH: Alzheimer Disease; drug therapy; pathology; physiopathology; Amyloid beta-Peptides; Angelica; chemistry; Animals; Brain; pathology; Brain-Derived Neurotrophic Factor; metabolism; Cognitive Dysfunction; complications; drug therapy; physiopathology; Cyclic AMP Response Element-Binding Protein; metabolism; Disease Models, Animal; Male; Maze Learning; drug effects; Memory, Short-Term; drug effects; Mice, Inbred C57BL; Neurogenesis; drug effects; Neuroglia; drug effects; metabolism; pathology; Neurons; drug effects; metabolism; pathology; Neuroprotective Agents; pharmacology; therapeutic use; Phosphorylation; drug effects; Phytotherapy; Plant Extracts; pharmacology; therapeutic use; Plaque, Amyloid; drug therapy; pathology; physiopathology; Signal Transduction; drug effects
- From: Chinese journal of integrative medicine 2018;24(5):378-384
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo research Angelica tenuissima Nakai (ATN) for use in novel Alzheimer's disease (AD) therapeutics.
METHODSThe 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 (Aβ) 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 Aβ-infused mice on the histopathological markers [neuronspecific nuclear protein (NeuN), Aβ] 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.
RESULTSKH032 treatment ameliorated cognitive impairments, reduced the overexpression of Aβ, and inhibited neuronal loss and neuroinflammatory response in the Aβ-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.
CONCLUSIONSKH032 attenuated cognitive defificits in the Aβ-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.
