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Abstract
Background Ulcerative colitis (UC) is a chronic nonspecific inflammatory disease of the colon and rectum. Recent studies found that berberine had effects on inflammatory diseases and immune diseases. Methods The PharmMapper database was used to predict the berberine potential target and GeneCards database and OMIM database were utilized to collect UC genes. The Cytoscape software was used to construct and analyze the networks and DAVID was utilized to perform enrichment analysis. Then, animal experiments were performed to validate the prediction results. The experimental rats were randomly divided into normal group (control group), model group, and berberine group. The general condition, body weight, gross morphology of colon tissue, and colonic mucosal damage index (CMDI) score were observed. The pathological changes of colon tissue were observed by H&E staining. The levels of serum interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and IL-4 were detected by ELISA. The expressions of IL-1β, TNF-α, and IL-4 protein in colon tissue were detected by immunohistochemistry. Results A total of 211 Berberine's potential targets and 210 UC genes were obtained. The enrichment analysis showed that berberine may regulate inflammation, inflammatory cytokines, and their mediated inflammation signal pathways such as inflammatory bowel disease (IBD), rheumatoid arthritis, cytokine-cytokine receptor interaction, TNF, T cell receptor, Toll-like receptor, and JAK/STAT signaling pathway. Compared with the model group, the body mass of rats in the berberine group was significantly increased (P < 0.05); the general morphology and pathological changes of colon tissue were significantly improved; CMDI score, serum and colon tissue IL-1β, TNF-α content, and protein expression were decreased significantly (P < 0.05); and IL-4 content and protein expression increased significantly (P < 0.05). Conclusion Berberine can interfere with UC through related biological processes and signal pathways related to inflammation and immunity. In-depth exploration of the mechanism of berberine in the treatment of UC will provide a basis for clinical application.
Highlights
Inflammatory bowel disease (IBD) mainly includes ulcerative colitis (UC) and Crohn’s disease (CD). e number of IBD patients in Europe and the United States has accounted for 0.5% of the world’s population
A total of 211 berberine’s potential targets and 210 UC genes were obtained. ere are some intersections between the berberine target set and the UC gene set (Figure 1(a)). e targets shared by the two target sets are MMP9, HRAS, STAT1, PRKCQ, MMP2, VDR, S100A9, IL2, PLA2G2A, ELANE, CTSG, PPARG, MMP3, AURKA, SRC, ALB, and BRAF
Berberine-UC protein-protein interaction (PPI) Network. is network is composed of 191 berberine potential target nodes, 151 UC gene nodes, 17 berberine-UC target nodes, and 6742 edges. e top 20 targets can be divided into three categories: (1) berberine target set: EGFR (140 edges), CASP3 (128 edges), and MAPK14 (113 edges); (2) UC gene set: IL-6 (185 edges), TNF (181 edges), AKT1 (173 edges), TP53 (163 edges), VEGFA (157 edges), STAT3 (146 edges), IL-10 (139 edges), TLR4 (133 edges), CXCL8 (128 edges), IL-1β (125 edges), PTGS2 (118 edges), and IL-4 (114 edges); and (3) berberine-UC target set: ALB (169 edges), MMP9 (126 edges), SRC (123 edges), IL-2 (120 edges), and HRAS (111 edges) (Figure 1(b))
Summary
Inflammatory bowel disease (IBD) mainly includes ulcerative colitis (UC) and Crohn’s disease (CD). e number of IBD patients in Europe and the United States has accounted for 0.5% of the world’s population. E main treatments for UC include the following: (1) Sulfasalazine salicylic acid preparations, such as Mesalazine; (2) corticosteroids, such as prednisone or dexamethasone; and (3) immunosuppressants [6, 7] These drugs are limited due to their limited clinical efficacy and large side effects. E enrichment analysis showed that berberine may regulate inflammation, inflammatory cytokines, and their mediated inflammation signal pathways such as inflammatory bowel disease (IBD), rheumatoid arthritis, cytokine-cytokine receptor interaction, TNF, T cell receptor, Toll-like receptor, and JAK/STAT signaling pathway. Compared with the model group, the body mass of rats in the berberine group was significantly increased (P < 0.05); the general morphology and pathological changes of colon tissue were significantly improved; CMDI score, serum and colon tissue IL-1β, TNF-α content, and protein expression were decreased significantly (P < 0.05); and IL-4 content and protein expression increased significantly (P < 0.05). In-depth exploration of the mechanism of berberine in the treatment of UC will provide a basis for clinical application
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