1. Tempeh attenuates cognitive deficit, antioxidant imbalance, and amyloid β of senescence-accelerated mice by modulating Nrf2 expression via MAPK pathway
- Author
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Bi-Chun Liang, Wen-Chin Yeh, I-Te Lee, Yin-Ching Chan, and Ming-Fu Wang
- Subjects
0301 basic medicine ,MAPK/ERK pathway ,Senescence ,medicine.medical_specialty ,Antioxidant ,Cognitive ,medicine.medical_treatment ,Medicine (miscellaneous) ,medicine.disease_cause ,Superoxide dismutase ,Tempeh ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Internal medicine ,medicine ,Amyloid precursor protein ,TX341-641 ,Nutrition and Dietetics ,biology ,Nutrition. Foods and food supply ,Senescence acceleration–prone mice ,Amyloid β ,Malondialdehyde ,030104 developmental biology ,Endocrinology ,chemistry ,Catalase ,biology.protein ,030217 neurology & neurosurgery ,Oxidative stress ,Food Science - Abstract
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 β (Aβ) and β-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 Aβ-induced damage and reduce memory impairment by modulating Nrf2 via mitogen-activated protein kinase pathway.
- Published
- 2018