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Protective effect of Phyllostachys edulis (Carrière) J. Houz against chronic ethanol-induced cognitive impairment in vivoopen accessProtective effect of Phyllostachys edulis (Carrière) J. Houz against chronic ethanol-induced cognitive impairment in vivo

Other Titles
Protective effect of Phyllostachys edulis (Carrière) J. Houz against chronic ethanol-induced cognitive impairment in vivo
Authors
Jiyeon KimJi Myung ChoiJi-Hyun Kim팡치치Jung Min OhJi Hyun KimHyun Young KimEun Ju Cho
Issue Date
Aug-2024
Publisher
한국영양학회
Keywords
Alcohol consumption; cognitive impairment; oxidative stress
Citation
Nutrition Research and Practice, v.18, no.4, pp 464 - 478
Pages
15
Indexed
SCIE
SCOPUS
KCI
Journal Title
Nutrition Research and Practice
Volume
18
Number
4
Start Page
464
End Page
478
URI
https://scholarworks.gnu.ac.kr/handle/sw.gnu/73564
DOI
10.4162/nrp.2024.18.4.464
ISSN
1976-1457
2005-6168
Abstract
BACKGROUND/OBJECTIVESChronic alcohol consumption causes oxidative stress in the body, which may accumulate excessively and cause a decline in memory; problem-solving, learning, and exercise abilities; and permanent damage to brain structure and function. Consequently, chronic alcohol consumption can cause alcohol-related diseases. MATERIALS/METHODSIn this study, the protective effects of Phyllostachys edulis (Carrière) J. Houz (PE) against alcohol-induced neuroinflammation and cognitive impairment were evaluated using a mouse model. Alcohol (16%, 5 g/kg/day for 6 weeks) and PE (100, 250, and 500 mg/kg/day for 21 days) were administered intragastrically to mice. RESULTSPE showed a protective effect against memory deficits and cognitive dysfunction caused by alcohol consumption, confirmed through behavioral tests such as the T-maze, object recognition, and Morris water maze tests. Additionally, PE attenuated oxidative stress by reducing lipid oxidation, nitric oxide, and reactive oxygen species levels in the mice’s brains, livers, and kidneys. Improvement of neurotrophic factors and downregulation of apoptosis-related proteins were confirmed in the brains of mice fed low and medium concentrations of PE. Additionally, expression of antioxidant enzyme-related proteins GPx-1 and SOD-1 was enhanced in the liver of PE-treated mice, related to their inhibitory effect on oxidative stress. CONCLUSIONThis suggests that PE has both neuroregenerative and antioxidant effects. Collectively, these behavioral and histological results confirmed that PE could improve alcohol-induced cognitive deficits through brain neurotrophic and apoptosis protection and modulation of oxidative stress.
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