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

  • Jiyeon Kim (Department of Food Science and Nutrition, Pusan National University) ;
  • Ji Myung Choi (Department of Food and Nutrition, Kyungsung University) ;
  • Ji-Hyun Kim (Department of Food Science and Nutrition, Pusan National University) ;
  • Qi Qi Pang (Department of Food Science and Nutrition, Pusan National University) ;
  • Jung Min Oh (Department of Food Science and Nutrition, Pusan National University) ;
  • Ji Hyun Kim (Department of Food Science and Nutrition, Gyeongsang National University) ;
  • Hyun Young Kim (Department of Food Science and Nutrition, Gyeongsang National University) ;
  • Eun Ju Cho (Department of Food Science and Nutrition, Pusan National University)
  • Received : 2024.02.21
  • Accepted : 2024.05.09
  • Published : 2024.08.01

Abstract

BACKGROUND/OBJECTIVES: Chronic 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/METHODS: In 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. RESULTS: PE 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. CONCLUSION: This 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.

Keywords

References

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