Author/Authors :
Liu، Minghui نويسنده Department of TCM, China-Japan Union Hospital of Jilin University, Changchun, China Liu, Minghui , Dou، Yuchang نويسنده Department of TCM, China-Japan Union Hospital of Jilin University, Changchun, China Dou, Yuchang , Sun، Ran نويسنده Science Research Center, China-Japan Union Hospital of Jilin University, Changchun, China Sun, Ran , Zhang، Yonggui نويسنده Department of Gastroenterology, China-Japan Union Hospital of Jilin University, Changchun, China Zhang, Yonggui , Liu، Yansong نويسنده Department of TCM, China-Japan Union Hospital of Jilin University, Changchun, China Liu, Yansong
Abstract :
Alcoholic hepatitis (AH) is an acute manifestation of alcoholic liver disease with high mortality rates. Our aim was to study the molecular mechanisms of AH. The differentially expressed genes (DEGs) in liver between AH and control cases were identified by analyzing the GSE28619 microarray data using t-test. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways and Gene Ontology (GO) enrichment analyses were performed using DAVID online tool. The protein-protein interaction (PPI) network was constructed using Search Tool for the Retrieval of Interacting Genes (STRING) and the subnetwork was identified by BioNet. Both PPI network and subnetwork were visualized using the Cytoscape software. Total 908 DEGs (551 up- and 357 down-regulated DEGs) were obtained. The up-regulated DEGs were significantly enriched in 15 pathways and 112 GO biological processes. The down-regulated DEGs were significantly enriched in 22 pathways and 84 GO biological processes. The PPI network with 608 nodes and 2878 interactions was constructed and the subnetwork with 53 nodes and 131 interactions was also identified. The hub DEGs (, , and ) were extracted in this subnetwork. TSPO might contribute to the liver damage and AH progression induced by mitochondrial dysfunction through oxidative stress of liver. TSPO interacted with PPIB might play important roles in liver damage in AH. The interaction between and might contribute to the transformation from AH to hepatocellular carcinoma.
