Hepatoprotective effects of IL-22 on fulminant hepatic failure induced by D-galactosamine and lipopolysaccharide in mice

被引:60
作者
Xing, Wei-Wei [1 ]
Zou, Min-ji [1 ]
Liu, Shen [1 ]
Xu, Tao [1 ]
Gao, Jie [1 ]
Wang, Jia-xi [1 ]
Xu, Dong-gang [1 ]
机构
[1] Inst Basic Med Sci, Mol Genet Lab, Beijing 100850, Peoples R China
关键词
Fulminant hepatic failure; Interleukin-22; Oxidative stress; Apoptosis; TNF-alpha; NECROSIS-FACTOR-ALPHA; LIVER-INJURY; OXIDATIVE STRESS; REACTIVE OXYGEN; INTERLEUKIN-22; APOPTOSIS; PROTECTS; CELLS; MODEL; RATS;
D O I
10.1016/j.cyto.2011.07.022
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
Interleukin-22 (IL-22), a member of the IL-10 cytokine family that is produced by activated Th22, Th1 and Th17 cells as well as natural killer cells, plays an important role in increase of innate immunity, protection from damage and enhancement of regeneration. Here, we examined the effects of IL-22 on acute liver failure model induced by D-galactosamine (GalN) and lipopolysaccharide (LPS). Administration of recombinant human IL-22 (rhIL-22) reduced the death rate markedly and prevented mice from severe hepatic injury, as evidenced by decreased serum alanine aminotransferase (ALT) and total bilirubin (T.Bil) activity as well as improved histological signs in liver. Furthermore, IL-22 treatment decreased the hepatic malondialdehyde (MDA) contents and increased the reduced glutathione levels. Serum tumor necrosis factor alpha (TNF-alpha) level and hepatic caspase-3 activity were significantly lower in mice administrated with IL-22. Moreover, IL-22 treatment significantly enhanced activation of STAT3 and up-regulated the expression of Bc1-xL, heme oxygenase-1 (HO-1) and redox factor-1 (Ref-1) in the liver injury induced by GalN/LPS. Collectively, these data indicate that IL-22 can provide critical protection against GalN/LPS-induced liver injury through anti-apoptotic, anti-oxidant and anti-inflammatory actions. (C) 2011 Elsevier Ltd. All rights reserved.
引用
收藏
页码:174 / 179
页数:6
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