Acer okamotoanum improves cognition and memory function in A beta(25-35)-induced Alzheimer's mice model
- Authors
- Choi, Soo Yeon; Lee, Jaemin; Lee, Dong Gu; Lee, Sanghyun; Cho, Eun Ju
- Issue Date
- Feb-2017
- Publisher
- KOREAN SOC APPLIED BIOLOGICAL CHEMISTRY
- Keywords
- Acer okamotoanum; Amyloid beta(25-35) peptide; Alzheimer's disease; Cognition; Learning; Memory deficit; Oxidative stress
- Citation
- APPLIED BIOLOGICAL CHEMISTRY, v.60, no.1, pp 1 - 9
- Pages
- 9
- Journal Title
- APPLIED BIOLOGICAL CHEMISTRY
- Volume
- 60
- Number
- 1
- Start Page
- 1
- End Page
- 9
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/4881
- DOI
- 10.1007/s13765-016-0244-x
- ISSN
- 2468-0834
2468-0842
- Abstract
- We studied the effect of ethyl acetate (EA) fraction from Acer okamotoanum on cognitive improvement and protective abilities in amyloid beta (A beta)(25-35) peptide-injected Alzheimer's disease (AD) mice. EA was oral administration at 100 and 200 mg/kg/day during the 14 days. We studied the protective effect of EA against AD on the basis of behavioral tests including T-maze test, Novel object recognition test, and Morris water maze test. Control group injected with A beta(25-35) showed significant impairments in memory function. But the oral administration of EA (EA 100 and EA 200 groups) improved the cognition and memory function. In addition, EA against A beta(25-35) peptide has been shown to inhibit lipid peroxidation levels and nitric oxide production in tissues. Acetylcholinesterase (AChE) was elevated in the brain by A beta(25-35) peptide, whereas administration of EA (EA 100 and EA 200 groups) significantly decreased AChE level. Our results indicated that EA improves learning and long-term memory against A beta(25-35) peptide-caused deficit through attenuation of oxidative stress.
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