Fibroblast growth factor 21 protects mouse brain against D-galactose induced aging via suppression of oxidative stress response and advanced glycation end products formation

	Fibroblast growth factor 21 protects mouse brain against D-galactose induced aging via suppression of oxidative stress response and advanced glycation end products formation
	Yu, Yinhang 1; Bai, Fuliang 1; Wang, Wenfei 1,2; Liu, Yaonan 1; Yuan, Qingyan 1; Qu, Susu 4; Zhang, Tong 1; Tian, Guiyou 1; Li, Siming 1,3; Li, Deshan 1,2
刊名	PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR
	2015-06-01
卷号	133 期号:0 页码:122-131
关键词	FGF21 D-galactose Aging Oxidative stress AGEs Inflammation
ISSN号	0091-3057
英文摘要	Fibroblast growth factor 21 (FGF21) is a hormone secreted predominantly in the liver, pancreas and adipose tissue. Recently, it has been reported that FGF21-Transgenic mice can extend their lifespan compared with wild type counterparts. Thus, we hypothesize that FGF21 may play some roles in aging of organisms. In this study h-galactose (D-gal)-induced aging mice were used to study the mechanism that FGF21 protects mice from aging. The three-month-old Kunming mice were subcutaneously injected with D-gal (180 mg.kg(-1).d(-1)) for 8 weeks and administered simultaneously with FGF21 (1, 2 or 5 mg.kg(-1).d(-1)). Our results showed that administration of FGF21 significantly improved behavioral performance of D-gal-treated mice in water maze task and step-down test, reduced brain cell damage in the hippocampus, and attenuated the D-gal-induced production of MDA, ROS and advanced glycation end products (AGEs). At the same time, FGF21 also markedly renewed the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and total anti-oxidation capability (T-AOC), and decreased the enhanced total cholinesterase (TChE) activity in the brain of D-gal-treated mice. The expression of aldose reductase (AR), sorbitol dehydrogenase (SDH) and member-anchored receptor for AGEs (RAGE) declined significantly after FGF21 treatment. Furthermore, FGF21 suppressed inflamm-aging by inhibiting I kappa B alpha degradation and NF-kappa B p65 nuclear translocation. The expression levels of pro-inflammatory cytokines, such as TNF-alpha and IL-6, decreased significantly. In conclusion, these results suggest that FGF21 protects the aging mice brain from D-gal-induced injury by attenuating oxidative stress damage and decreasing AGE formation. (C) 2015 Elsevier Inc. All rights reserved.
收录类别	SCI
语种	英语
WOS记录号	WOS:000355883000015
内容类型	期刊论文
源URL	[http://ir.psych.ac.cn/handle/311026/13374]
专题	心理研究所_健康与遗传心理学研究室
作者单位	1.Northeast Agr Univ, Life Sci Coll, Biopharmaceut Lab, Harbin 150030, Peoples R China 2.Key Lab Agr Biol Funct Gene, Harbin 150030, Peoples R China 3.Harbin Univ Commerce, Harbin 150028, Peoples R China 4.Chinese Acad Sci, Inst Psychol, Beijing 100101, Peoples R China
推荐引用方式 GB/T 7714	Yu, Yinhang,Bai, Fuliang,Wang, Wenfei,et al. Fibroblast growth factor 21 protects mouse brain against D-galactose induced aging via suppression of oxidative stress response and advanced glycation end products formation[J]. PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR,2015,133(0):122-131.
APA	Yu, Yinhang.,Bai, Fuliang.,Wang, Wenfei.,Liu, Yaonan.,Yuan, Qingyan.,...&Ren, Guiping.(2015).Fibroblast growth factor 21 protects mouse brain against D-galactose induced aging via suppression of oxidative stress response and advanced glycation end products formation.PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR,133(0),122-131.
MLA	Yu, Yinhang,et al."Fibroblast growth factor 21 protects mouse brain against D-galactose induced aging via suppression of oxidative stress response and advanced glycation end products formation".PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR 133.0(2015):122-131.