Kim Min Jeong, Jung Ji Eun, Lee Sanghyun, Cho Eun Ju, Kim Hyun Young
Department of Food Science and Nutrition, Pusan National University, Busan 46241, Korea.
Department of Plant Science and Technology, Chung-Ang University, Anseong 17546, Korea.
Nutr Res Pract. 2021 Apr;15(2):173-186. doi: 10.4162/nrp.2021.15.2.173. Epub 2020 Sep 25.
BACKGROUD/OBJECTIVES: Alzheimer's disease (AD) is the most common cause of dementia in the elderly. Due to the increased incidence of dementia, there is a corresponding increase concerning the importance of AD. In this study, we investigated the protective effects conferred by (Zj) and fermented by yeast (Zj-Y), on cognitive impairment in an AD mouse model.
MATERIALS/METHODS: AD was induced by injecting amyloid beta (Aβ) in ICR mice, and subsequently 200 mg/kg Zj or Zj-Y was administered daily for 14 days. The cognitive ability of AD mice was observed through behavioral experiments in T-maze, novel object recognition, and Morris water maze tests. We subsequently measured the levels of malondialdehyde (MDA), nitric oxide (NO), aspartate aminotransferase, and alanine aminotransferase in either tissues or serum.
In behavioral tests, deterioration was revealed in the short- and long-term learning and memory functions in the Aβ-injected control group compared to the normal group, indicating that Aβ injection impairs cognitive functions. However, administration of Zj and Zj-Y improved cognitive function in mice, as compared to the Aβ-injected control mice. In addition, the Aβ induced elevations of MDA and NO in the brain, kidney, and liver were suppressed after exposure to Zj and Zj-Y. Especially, Zj-Y showed stronger scavenging effect against MDA and NO, as compared to Zj.
Results of the present study indicate that Zj-Y exerts a protective effect on cognitive impairment and memory dysfunction, which is exerted by attenuating the oxidative stress induced by Aβ.
背景/目的：阿尔茨海默病（AD）是老年人痴呆最常见的病因。由于痴呆发病率上升，AD的重要性也相应增加。在本研究中，我们调查了[具体物质1]（Zj）和经酵母发酵的[具体物质1]（Zj - Y）对AD小鼠模型认知障碍的保护作用。
材料/方法：通过向ICR小鼠注射β淀粉样蛋白（Aβ）诱导AD，随后每天给予200mg/kg Zj或Zj - Y，持续14天。通过T迷宫、新物体识别和莫里斯水迷宫试验中的行为实验观察AD小鼠的认知能力。随后我们测量了组织或血清中丙二醛（MDA）、一氧化氮（NO）、天冬氨酸转氨酶和丙氨酸转氨酶的水平。
在行为测试中，与正常组相比，注射Aβ的对照组短期和长期学习及记忆功能均出现衰退，表明注射Aβ会损害认知功能。然而，与注射Aβ的对照小鼠相比，给予Zj和Zj - Y可改善小鼠的认知功能。此外，暴露于Zj和Zj - Y后，Aβ诱导的脑、肾和肝脏中MDA和NO的升高受到抑制。特别是，与Zj相比，Zj - Y对MDA和NO的清除作用更强。
本研究结果表明，Zj - Y对认知障碍和记忆功能障碍具有保护作用，其作用机制是减轻Aβ诱导的氧化应激。
