动物造模 z-bio 2022-12-07 312

　　Objective To detect the changes of gene expression in colon tissue of mice with inflammatory bowel disease (IBD) by transcriptome sequencing, and to improve the understanding of the molecular mechanism of mesalazine in the treatment of IBD.

　　Methods The IBD mouse model was established with dextran sulfate sodium. Fifteen C57BL/6 mice were randomly divided into three groups: control group, DSS group and DSS+5-ASA group. Three mice in each group were randomly selected to take colon tissues for sequencing, and the differential expression genes and important biological signal pathways were identified by comparison between the two groups. Subsequently, the sub significant DEGs identified previously were validated by microarray data from colonic biopsy of patients with ulcerative colitis and patients after mesalazine treatment in the gene expression database.

　　Results There were 2983 differentially expressed genes, 604 up-regulated genes and 753 down-regulated genes in DSS+5-ASA group compared with DSS group; Compared with the control group, the DSS group obtained 1626 differentially expressed genes, including 820 up-regulated genes and 806 down-regulated genes. The enrichment analysis results of GO (gene ontology) and KEGG showed that these DEGs were related to signal pathways such as immune response. Some genes with significant expression differences, such as Rnase1 and Cxcl10, have similar expression trends in colon tissues of UC patients.

　　Conclusion The gene expression profile of colon tissue of IBD model mice treated with mesalazine was verified by comparison with IBD patients, and several genes and biological pathways that may be involved in the treatment of IBD were obtained, which increased the further understanding of the therapeutic mechanism of mesalazine on IBD.