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 Kim; Ji Myung Choi; Ji-Hyun Kim; 팡치치; Jung Min Oh; Ji Hyun Kim; Hyun Young Kim; Eun 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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