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Quercetin ameliorates learning and memory via the Nrf2-ARE signaling pathway in D-galactose-induced neurotoxicity in mice
被引:87
作者:
Dong, Fuxing
[1
]
Wang, Shuang
[2
]
Wang, Yiwen
[2
]
Yang, Xiao
[2
]
Jiang, Jiali
[2
]
Wu, Dejian
[2
]
Qu, Xuebin
[1
]
Fan, Hongbin
[3
]
Yao, Ruiqin
[1
]
机构:
[1] Xuzhou Med Univ, Res Ctr Neurobiol, 209 Tongshan Rd, Xuzhou 221004, Jiangsu, Peoples R China
[2] Xuzhou Med Univ, Anesthesiol Dept, 209 Tongshan Rd, Xuzhou 221004, Jiangsu, Peoples R China
[3] Xuzhou Med Univ, Affiliated Hosp, Dept Neurol, 99 Huaihai West Rd, Xuzhou 221002, Jiangsu, Peoples R China
关键词:
Quercetin;
Mouse brain aging;
D-galactose;
Morris water maze;
Apoptosis Nrf2-ARE;
INDUCED COGNITIVE DEFICITS;
RAT-BRAIN;
IMPAIRMENT;
APOPTOSIS;
DISEASE;
STRESS;
DAMAGE;
MODEL;
DNA;
D O I:
10.1016/j.bbrc.2017.07.151
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Aging is accompanied by deficits in cognitive function and neuronal degeneration or loss. Quercetin is a flavonoid that exhibits powerful antioxidant activity. This study evaluated the protective effects and mechanisms of quercetin in D-galactose-induced neurotoxicity in mice. Quercetin was administered daily at doses of 20 or 50 mg/kg in D-galactose-injected (50mg/kg/subcutaneous (s.c.)) mice for eight weeks. Morris water maze tests demonstrated that quercetin significantly improved learning and memory compared to o D-galactose-treated control mice. Quercetin also prevented changes in the neuronal cell morphology and apoptosis in the hippocampus as well as increased the expression of Nrf2, HO-1 and SOD in o -galactose-treated mice. Treatment with the Nrf2 inhibitor Brusatol reversed the effects of quercetin on HO-1 and SOD expression as well as neuronal cell protection. In conclusion, quercetin protected mice from o -galactose-induced cognitive functional impairment and neuronal cell apoptosis via activation of the Nrf2-ARE signaling pathway. (C) 2017 Elsevier Inc. All rights reserved.
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页码:636 / 641
页数:6
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