ArticleFrontiers in genetics2021
Comparative Transcriptomic Analysis Reveals the Immunosuppressive Targets of Mesalazine in Dextran Sulfate Sodium-Induced Ulcerative Colitis.
Article in Frontiers in genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Integrated Multi-Omics Analysis Reveals Activation of the PPAR Signaling Pathway by Koumiss in Experimental Ulcerative Colitis.International journal of molecular sciences · 2026Article
- Carrier-free supramolecular architectonics of quercetinMaterials today. Bio · 2026Article
- Short-term caloric restriction partially reprograms immune and microbial networks during acute DSS-induced colitis.Genes & nutrition · 2026Article
- Mesalazine RegulatesPharmaceutics · 2025Article
- Patchoulene epoxide mitigates colitis and hepatic damage induced by dextran sulfate sodium by regulating the colonic microbiota and purine metabolism.Frontiers in immunology · 2025Article
- Berberine inhibits IFN-γ signaling pathway in DSS-induced ulcerative colitis.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2022Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
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Abstract
Ulcerative colitis (UC) is a complex inflammatory bowel disorder that can induce colonic and rectal dysfunction. Mesalazine, a first-line medicine, is routinely prescribed for UC treatment. However, the pharmacological targets of mesalazine against UC are not detailed in current publications. In the current study, a transcriptomics strategy was applied to reveal the therapeutic targets and molecular mechanisms of mesalazine for treating dextran sulfate sodium (DSS)-induced UC in mice. Compared with the UC group, a total of 1,663 differentially expressed genes were identified in mesalazine-treated mice, of which 262 were upregulated and 1,401 were downregulated. GO and KEGG enrichment analyses indicated that the protective actions of mesalazine for treating UC were related to the functional regulation of immune inflammatory response, such as the regulation of T cells, white blood cells, and cytokine receptor pathways. In addition, ingenuity pathway analysis of the gene network further revealed the inhibitory action of mesalazine on C-C motif chemokine ligands (CCL11 and CCL21) and C-X-C motif chemokine ligands (CXCL3 and CXCR2). Taken together, the current transcriptomic findings revealed anti-UC pharmacological targets, including the newly discovered biotargets CCL11, CCL21, CXCL3, and CXCR2, of mesalazine against DSS-induced intestinal inflammation.
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