Kim Jiyeon, Choi Ji Myung, Kim Ji-Hyun, Pang Qi Qi, Oh Jung Min, Kim Ji Hyun, Kim Hyun Young, Cho Eun Ju
Department of Food Science and Nutrition, Pusan National University, Busan 46241, Korea.
Department of Food and Nutrition, Kyungsung University, Busan 48434, Korea.
Nutr Res Pract. 2024 Aug;18(4):464-478. doi: 10.4162/nrp.2024.18.4.464. Epub 2024 May 16.
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 (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.
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 and was enhanced in the liver of PE-treated mice, related to their inhibitory effect on oxidative stress.
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.
背景/目的：长期饮酒会导致体内氧化应激，这种应激可能过度积累，导致记忆力下降；解决问题、学习和运动能力下降；以及对大脑结构和功能的永久性损害。因此，长期饮酒会引发与酒精相关的疾病。
材料/方法：在本研究中，使用小鼠模型评估了（卡里埃）J. 胡兹（PE）对酒精诱导的神经炎症和认知障碍的保护作用。给小鼠灌胃酒精（16%，5克/千克/天，持续6周）和PE（100、250和500毫克/千克/天，持续21天）。
通过T迷宫、物体识别和莫里斯水迷宫等行为测试证实，PE对饮酒引起的记忆缺陷和认知功能障碍具有保护作用。此外，PE通过降低小鼠大脑、肝脏和肾脏中的脂质氧化、一氧化氮和活性氧水平来减轻氧化应激。在喂食低、中浓度PE的小鼠大脑中，证实了神经营养因子的改善和凋亡相关蛋白的下调。此外，PE处理小鼠的肝脏中抗氧化酶相关蛋白和的表达增强，这与其对氧化应激的抑制作用有关。
这表明PE具有神经再生和抗氧化作用。总的来说，这些行为和组织学结果证实，PE可以通过脑神经营养、凋亡保护和氧化应激调节来改善酒精诱导的认知缺陷。
