Protective effects of recombinant human cytoglobin against chronic alcohol-induced liver disease in vivo and in vitro.

Abstract	Alcoholic liver disease (ALD) is an important worldwide public health issue with no satisfying treatment available since now. Here we explore the effects of recombinant human cytoglobin (rhCygb) on chronic alcohol-induced liver injury and the underlying mechanisms. In vivo studies showed that rhCygb was able to ameliorate alcohol-induced liver injury, significantly reversed increased serum index (ALT, AST, TG, TC and LDL-C) and decreased serum HDL-C. Histopathology observation of the liver of rats treated with rhCygb confirmed the biochemical data. Furthermore, rhCygb significantly inhibited Kupffer cells (KCs) proliferation and TNF-α expression in LPS-induced KCs. rhCygb also inhibited LPS-induced NADPH oxidase activity and ROS, NO and O2•- generation. These results collectively indicate that rhCygb exert the protective effect on chronic alcohol-induced liver injury through suppression of KC activation and oxidative stress. In view of its anti-oxidative stress and anti-inflammatory features, rhCygb might be a promising candidate for development as a therapeutic agent against ALD.
Authors	Jian Wen, Yongbin Wu, Wei Wei, Zhen Li, Ping Wang, Shiwei Zhu, Wenqi Dong
Journal	Scientific reports (Sci Rep) Vol. 7 Pg. 41647 (01 27 2017) ISSN: 2045-2322 [Electronic] England
PMID	28128325 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References	Biomarkers CYGB protein, human Cygb protein, rat Cytoglobin Lipopolysaccharides Protective Agents Reactive Oxygen Species Recombinant Proteins Tumor Necrosis Factor-alpha Globins
Topics	Animals Biomarkers Cell Proliferation (drug effects) Cytoglobin Disease Models, Animal Globins (pharmacology) Humans Kupffer Cells (drug effects, metabolism) Lipopolysaccharides (adverse effects) Liver (drug effects, metabolism, pathology) Liver Diseases, Alcoholic (drug therapy, metabolism, pathology) Liver Function Tests Male Oxidation-Reduction Oxidative Stress (drug effects) Protective Agents (pharmacology) Rats Reactive Oxygen Species (metabolism) Recombinant Proteins (pharmacology) Tumor Necrosis Factor-alpha (metabolism)

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