动物造模 z-bio 2023-02-23 466

　　Objective To use transcriptome sequencing technology to detect the changes of gene expression in colon tissue of mice with inflammatory bowel disease, 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 were randomly selected from each group to take colon tissue for sequencing, and the differentially expressed genes and important biological signaling pathways were identified by comparison between the two groups. The previously identified sub-significant DEGs were subsequently validated by microarray data from colonic biopsies of ulcerative colitis patients and mesalazine-treated patients in the gene expression database.

　　Results A total of 2983 differentially expressed genes were obtained between the DSS+5-ASA group and the DSS group, including 604 up-regulated genes and 753 down-regulated genes; compared with the control group, a total of 1626 differentially expressed genes were obtained in the DSS group, including 820 up-regulated genes and 753 down-regulated genes. 806 genes were down-regulated. GO and KEGG enrichment analysis showed that these DEGs were related to signaling pathways such as immune response. Some genes with significant differences in expression, such as Rnase1 and Cxcl10, have similar expression trends in colon tissue of UC patients.

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