1. Naringenin Ameliorates Behavioral Dysfunction and Neurological Deficits in a d-Galactose-Induced Aging Mouse Model Through Activation of PI3K/Akt/Nrf2 Pathway.
- Author
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Zhang, Yan, Liu, Bin, Chen, Xi, Zhang, Ning, Li, Guang, Zhang, Li-Hong, Tan, Li-Yan, Li-Hong Zhang, Li-Hong, and Li-Yan Tan, Li-Yan
- Subjects
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NARINGENIN , *BEHAVIOR disorders , *NEUROLOGICAL disorders , *LABORATORY mice , *PROTEIN kinase B , *OXIDATIVE stress , *GALACTOSE , *PROTEIN metabolism , *AGING , *ANIMAL behavior , *ANIMAL experimentation , *ANTHROPOMETRY , *APOPTOSIS , *BIOLOGICAL models , *BODY weight , *BRAIN , *CELLULAR signal transduction , *MEMORY , *MICE , *MOLECULAR structure , *MOTOR ability , *NEURONS , *OXIDATION-reduction reaction , *PHOSPHOTRANSFERASES , *SPATIAL behavior , *TRANSFERASES , *HEXOSES , *FLAVANONES , *PHARMACODYNAMICS - Abstract
In this study, we evaluated the protective effects of naringenin on aging mice induced by d-galactose (d-gal). Open field test and Morris water maze test were performed to evaluate the effect of naringenin on behavioral dysfunction. Hematoxylin-eosin staining, TUNEL staining, and Nissl staining were used to estimate the effect of naringenin on neurological deficits. Furthermore, naringenin markedly activated PI3K/Akt signaling, eventually promoted the nuclear translocation of nuclear factor-erythroid 2-related factor 2, and induced the expression of heme oxygenase 1 and NAD(P)H-quinone oxidoreductase 1. Superoxide dismutase (SOD), catalase (CAT), and thiobarbituric acid reactive substances (TBARS) assays were conducted to evaluate oxidative stress in d-gal-induced aging mice. Our finding demonstrated that naringenin was a promising agent for attenuating the aging process, and enhancing endogenous antioxidant defense capacity was a reliable strategy to delay the senescence process. [ABSTRACT FROM AUTHOR]
- Published
- 2017
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