Objective: How to find the specific target of spleen, kidney and renal dysfunction?
Method: 96 Wistar rats were randomly divided into model group, high-dose group, middle-dose group, low-dose group and SASP group. Give the corresponding drugs to the treatment group. Mandatory oral? Have you selected blank and model colon tissues for high-throughput sequencing? T? Is the gene expression of the selected chemokine detected using qPCR?
Result: Compared with the model group of rats, ask? Value ≤0.0 times? Do you want to screen the differentially expressed genes in the blank group based on changes ≥ 1.5? Does GO functional classification analysis show that differential gene functions are mainly enriched in biological processes (BP)? Cell component (cell component (CC)? Molecular function (MF) 3 levels? Differential gene KEGG enrichment analysis significantly up-regulates the expression of CXCL1? CXCL2? CXCR2? CXCL6? CCL7? CCL12 genes in the chemokine signaling pathway. QPCR It is confirmed that the gene expression changes of the above factors are consistent with the sequencing results. Is the expression of the above factors significantly down-regulated in Pire Decoction and after treatment?
Conclusion: CXCL1? The expression of CXCL6, CCL7 and CCL12 genes in the chemokine signaling pathway of ulcerative colitis with defects of spleen and kidney, CXCL2, CXCR2, and kidney are significantly up-regulated, which can be used as an objective indicator of UC mucosal inflammation. And the kidney can effectively down-regulate the expression of the above factors, and can delay the inflammatory response and promote the repair of the damaged colonic mucosa?