期刊
LABORATORY INVESTIGATION
卷 95, 期 5, 页码 504-514出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/labinvest.2015.34
关键词
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资金
- National Natural Science Foundation of China [81072766]
- Beijing Natural Science Foundation [7112066]
- 215 Program from Beijing Municipal Health Bureau [2013-2-11]
Saccharides are reported to protect hepatocytes from acute liver injury through distinct mechanisms. To date, the protective role of galactose against acute liver injury induced by lipopolysaccharide (LPS) and D-galactosamine (D-GalN) has been attributed to competition with D-GalN. Here, we showed that in addition to its effects on LPS/D-GalN and tumor necrosis factor alpha (TNF-alpha)/D-GalN models, galactose improves hepatic injury in mice challenged with LPS alone or TNF-alpha/actinomycin D. Consistent with this result, galactose enhanced the viability of TNF-alpha-stimulated Chang Liver and Hu7.5 hepatic cell lines. Specifically, galactose prevented TNF-alpha-induced apoptosis of hepatocytes through promoting phosphorylation of nuclear factor kappa B (NF-kappa B) p65. Additionally, galactose enhanced expression of the anti-apoptotic genes, c-IAP1 and A20, and inhibited cleavage of caspase-8 and caspase-3. These findings collectively suggest that galactose prevents TNF-alpha-induced liver injury through activation of the NF-kappa B signaling pathway. Considering that monosaccharides protect against liver injury via distinct mechanisms, these compounds may represent a promising clinical approach to treat acute liver failure.
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