PSYCH OpenIR  > 健康与遗传心理学研究室
Fibroblast growth factor (FGF21) protects mouse liver against D-galactose-induced oxidative stress and apoptosis via activating Nrf2 and PI3K/Akt pathways
Yu, Yinhang1; Bai, Fuliang1; Liu, Yaonan1; Yang, Yongbi1; Yuan, Qingyan1; Zou, Dehua2; Qu, Susu3; Tian, Guiyou1; Song, Liying1; Zhang, Tong1; Li, Siming4; Liu, Yunye1; Wang, Wenfei1,5; Ren, Guiping1,5; Li, Deshan1,5
2015-05-01
发表期刊MOLECULAR AND CELLULAR BIOCHEMISTRY
ISSN0300-8177
文章类型Article
卷号403期号:1-2页码:287-299
摘要FGF21 is recently discovered with pleiotropic effects on glucose and lipid metabolism. However, the potential protective effect of FGF21 against D-gal-induced injury in the liver has not been demonstrated. The aim of this study is to investigate the pathophysiological role of FGF21 on hepatic oxidative injury and apoptosis in mice induced by D-gal. The 3-month-old Kunming mice were subcutaneously injected with D-gal (180 mg kg(-1) d(1)) for 8 weeks and administered simultaneously with FGF21 (5 or 1 mg kg(-1) d(1)). Our results showed that the administration of FGF21 significantly alleviated histological lesion including structure damage, degeneration, and necrosis of hepatocytes induced by D-gal, and attenuated the elevation of liver injury markers, serum AST, and ALP in a dosedependent manner. FGF21 treatment also suppressed D-galinduced profound elevation of ROS production and oxidative stress, as evidenced by an increase of the MDA level and depletion of the intracellular GSH level in the liver, and restored the activities of antioxidant enzymes SOD, CAT, GSH-Px, and T-AOC. Moreover, FGF21 treatment increased the nuclear abundance of Nrf2 and subsequent up regulation of several antioxidant genes. Furthermore, a TUNEL assay showed that D-gal-induced apoptosis in the mouse liver was significantly inhibited by FGF21. The expression of caspase-3 was markedly inhibited by the treatment of FGF21 in the liver of D-gal-treated mice. The levels of PI3K and PBK/Akt were also largely enhanced, which in turn inactivated pro-apoptotic signaling events, restoring the balance between pro-and anti-apoptotic Bcl-2 and Bax proteins in the liver of D-gal-treated mice. In conclusion, these results suggest that FGF21 protects the mouse liver against D-gal-induced hepatocyte oxidative stress via enhancing Nrf2-mediated antioxidant capacity and apoptosis via activating PI3K/Akt pathway.
关键词FGF21 D-Gal Nrf2-mediated antioxidant capacity PI3K/AKT Apoptosis
收录类别SCI
语种英语
WOS记录号WOS:000355432700028
引用统计
文献类型期刊论文
条目标识符http://ir.psych.ac.cn/handle/311026/13375
专题健康与遗传心理学研究室
作者单位1.Northeast Agr Univ, Biopharmaceut Lab, Life Sci Coll, Harbin 150030, Peoples R China
2.Heilongjiang Bayi Agr Univ, Daqing 163319, Peoples R China
3.Chinese Acad Sci, Inst Psychol, Beijing 100101, Peoples R China
4.Harbin Univ Commerce, Harbin 150028, Peoples R China
5.Northeast Agr Univ, Key Lab Agr Biol Funct Gene, Harbin 150030, Peoples R China
推荐引用方式
GB/T 7714
Yu, Yinhang,Bai, Fuliang,Liu, Yaonan,et al. Fibroblast growth factor (FGF21) protects mouse liver against D-galactose-induced oxidative stress and apoptosis via activating Nrf2 and PI3K/Akt pathways[J]. MOLECULAR AND CELLULAR BIOCHEMISTRY,2015,403(1-2):287-299.
APA Yu, Yinhang.,Bai, Fuliang.,Liu, Yaonan.,Yang, Yongbi.,Yuan, Qingyan.,...&Li, Deshan.(2015).Fibroblast growth factor (FGF21) protects mouse liver against D-galactose-induced oxidative stress and apoptosis via activating Nrf2 and PI3K/Akt pathways.MOLECULAR AND CELLULAR BIOCHEMISTRY,403(1-2),287-299.
MLA Yu, Yinhang,et al."Fibroblast growth factor (FGF21) protects mouse liver against D-galactose-induced oxidative stress and apoptosis via activating Nrf2 and PI3K/Akt pathways".MOLECULAR AND CELLULAR BIOCHEMISTRY 403.1-2(2015):287-299.
条目包含的文件
文件名称/大小 文献类型 版本类型 开放类型 使用许可
WOS_000355432700028.(4927KB)期刊论文出版稿暂不开放CC BY-NC-SA请求全文
个性服务
推荐该条目
保存到收藏夹
查看访问统计
导出为Endnote文件
谷歌学术
谷歌学术中相似的文章
[Yu, Yinhang]的文章
[Bai, Fuliang]的文章
[Liu, Yaonan]的文章
百度学术
百度学术中相似的文章
[Yu, Yinhang]的文章
[Bai, Fuliang]的文章
[Liu, Yaonan]的文章
必应学术
必应学术中相似的文章
[Yu, Yinhang]的文章
[Bai, Fuliang]的文章
[Liu, Yaonan]的文章
相关权益政策
暂无数据
收藏/分享
所有评论 (0)
暂无评论
 

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。