Tempeh attenuates cognitive deficit, antioxidant imbalance, and amyloid β of senescence-accelerated mice by modulating Nrf2 expression via MAPK pathway

被引:17
|
作者
Chan, Yin-Ching [1 ]
Lee, I-Te [2 ]
Wang, Ming-Fu [1 ]
Yeh, Wen-Chin [1 ]
Liang, Bi-Chun [1 ]
机构
[1] Providence Univ, Dept Food & Nutr, 200,Sec 7,Taiwan Blvd, Taichung 43301, Taiwan
[2] Taichung Vet Gen Hosp, Div Endocrinol & Metab, Taichung, Taiwan
关键词
Tempeh; Senescence acceleration-prone mice; Cognitive; Antioxidant; Amyloid beta; GAMMA-AMINOBUTYRIC-ACID; DISEASE-LIKE PATHOLOGY; ALZHEIMERS-DISEASE; OXIDATIVE STRESS; GENE-EXPRESSION; CELL-SURVIVAL; MOUSE SAMP8; IN-VITRO; MODEL; MEMORY;
D O I
10.1016/j.jff.2018.09.023
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
This study investigated the effects of tempeh on the cognitive and antioxidant status in senescence-accelerated mouse prone 8 (SAMP8) mice. Six-month-old SAMP8 mice were divided into one control and three tempeh groups; the tempeh groups were administered 300, 600, and 900 mg/kg body weight (BW) tempeh. The results revealed tempeh groups had stronger cognitive ability, lower malondialdehyde and carbonyl protein levels, and higher superoxide dismutase (SOD) and catalase (CAT) activities in the hippocampus, striatum, and cortex. Of them, the 900 mg/kg BW tempeh showed the most superior results on increasing SOD and CAT mRNA expressions and reducing amyloid beta (A beta) and beta-site amyloid precursor protein cleaving enzyme 1 levels; it also increased nuclear factor erythroid 2-related factor 2 (Nrf2) levels by reducing p-p38 and p-JNK expression. In conclusion, tempeh may protect neurons against oxidative stress and A beta-induced damage and reduce memory impairment by modulating Nrf2 via mitogen-activated protein kinase pathway.
引用
收藏
页码:112 / 119
页数:8
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