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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
Source PublicationMOLECULAR AND CELLULAR BIOCHEMISTRY
ISSN0300-8177
SubtypeArticle
Volume403Issue:1-2Pages:287-299
AbstractFGF21 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.
KeywordFGF21 D-Gal Nrf2-mediated antioxidant capacity PI3K/AKT Apoptosis
Indexed BySCI
Language英语
WOS IDWOS:000355432700028
Citation statistics
Cited Times:35[WOS]   [WOS Record]     [Related Records in WOS]
Document Type期刊论文
Identifierhttp://ir.psych.ac.cn/handle/311026/13375
Collection健康与遗传心理学研究室
Affiliation1.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
Recommended Citation
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.
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