Label-free quantitative proteomics and bioinformatics analyses of alcoholic liver disease in a chronic and binge mouse model

As a significant cause of mortality and morbidity, alcoholic liver disease (ALD) has been widely investigated. However, little is known about the underlying metabolic mechanisms involved in the complicated pathological processes of ALD. The present study used label-free quantitative proteomics and bioinformatics analyses to investigate the differentially expressed proteins (DEPs) and their functions in the livers of alcohol-feed (AF) and control pair-feed (PF) mice. As a result, 87 upregulated DEPs and 133 downregulated DEPs were identified in AF liver tissues compared with PF livers. Gene ontology and Kyoto encyclopedia of genes and genomes bioinformatics analyses demonstrated that the DEPs were significantly enriched in ‘protein binding’, ‘metabolism’, ‘signal conduction’ and ‘immune response’. The expression of several core proteins including thyroid hormone receptor interactor 12 (TRIP12), NADH dehydrogenase (ubiquinone)1 α subcomplex, assembly factor 3 (NDUFAF3) and guanine monophosphate synthetase (GMPS) was validated by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) in a larger series of samples. The RT-qPCR results confirmed that TRIP12, NDUFAF3 and GMPS genes were significantly differentially expressed in between the AF and PF samples. These results extend our understanding of the molecular mechanisms underlying the occurrence and development of ALD. The present study indicated that the majority of DEPs serve vital roles in multiple metabolic pathways and this extends our knowledge of the molecular mechanisms involved in the occurrence and progression of ALD.