OBJECTIVE: Inflammatory bowel diseases (IBDs) including ulcerative colitis (UC) and Crohn's disease (CD) increased the risk for developing colorectal cancer. However, there is no effective therapy for IBDs. The aim of this study was to identify potential therapeutic targets for inflammatory bowel disease (IBD) and explore the possible mechanism underlying this disease. MATERIALS AND METHODS: Gene expression profile GSE6731 was downloaded from Gene Expression Omnibus database, which included 9 UC samples and 19 CD samples. Differentially expressed genes (DEGs) between affected colon tissues and non-affected tissues were identified in UC and CD group. Then, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways analysis of DEGs were performed. Modules in the protein-protein interaction (PPI) network were identified, and significant node genes were selected. RESULTS: Total 619 DEGs including 285 up-regulated genes and 334 down-regulated genes were identified in UC group and total 1159 DEGs of CD including 585 up-regulated genes and 574 down-regulated genes were selected. Module was selected from PPI network. From the PPI network and module, DEGs of mitogen-activated protein kinase 3 (MAPK3), N-myc downstream regulated 1 (NDRG1) and major histocompatibility complex, class II, DR alpha (HLA-DRA) have high degree. CONCLUSIONS: MAPK3, NDRG1 and HLA-DRA may play key roles in the progression and development of IBD. They may be used as specific therapeutic targets in the treatment of IBD. However, further experiments are still needed to confirm our results.