Literature DB >> 32450383

Dihydroartemisinin ameliorates dextran sulfate sodium induced inflammatory bowel diseases in mice.

Zili Lei1, Yanhong Yang2, Shaomin Liu3, Yuting Lei1, Lanxiang Yang3, Xueying Zhang3, Wanwan Liu1, Huijuan Wu3, Changyuan Yang3, Jiao Guo4.   

Abstract

In the present study, the effects of dihydroartemisinin (DHA) on inflammatory bowel diseases (IBD) mice model induced by dextran sulfate sodium (DSS) were determined. Hematoxylin and eosin staining was used to assess the intestines of mice treated with DSS and DHA. The expression of inflammatory factors and cell junction-associated genes was measured using reverse transcription-quantitative PCR (RT-qPCR) and Western blot. The effects of DSS and DHA on the gut microbiome were measured using 16S recombinant (r) DNA gene analysis. DHA could improve the diarrhea and bloody stool induced by DSS, and decrease the serum levels of TNF-α, IL-1β and IL-23 of the DSS group. DHA could notably reduce the infiltration of the inflammatory cells and significantly decrease the expression of TNF-α and IL-1β in the intestines of the DSS treated mice. The expression of cell junction-associated genes such as EpCAM and Claudins, were down-regulated in the DSS group, and DHA could recover the expression of these cell junction-associated genes. The 16S rDNA gene analysis demonstrated that Bacteroidetes and Verrucomicrobia decreased, while Firmicutes and Proteobacteria increased in the DSS group, and DHA could recover the abundance of these gut bacteria altered by DSS. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis revealed that DHA could partly recover the pathways altered by DSS. DHA could obviously ameliorate the symptoms of IBD induced by DSS by regulation of the expression of inflammation and cell junction-associated genes and gut microbiota, suggesting its potential for the treatment of IBD.
Copyright © 2020 Elsevier Inc. All rights reserved.

Entities:  

Keywords:  Adherens junction; Dextran sulfate sodium; Dihydroartemisinin; Gut microbiome; Inflammation; Inflammatory bowel diseases; Tight junction

Mesh:

Substances:

Year:  2020        PMID: 32450383     DOI: 10.1016/j.bioorg.2020.103915

Source DB:  PubMed          Journal:  Bioorg Chem        ISSN: 0045-2068            Impact factor:   5.275


  7 in total

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2.  Dihydroartemisinin Inhibits TGF-β-Induced Fibrosis in Human Tenon Fibroblasts via Inducing Autophagy.

Authors:  Xiaoyuan Wang; Wuqi Song; Fengmin Zhang; Renping Huang
Journal:  Drug Des Devel Ther       Date:  2021-03-03       Impact factor: 4.162

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Authors:  Bo Zhang; Xiang Chen; Yu Gan; Bing-Sheng Li; Kang-Ning Wang; Yao He
Journal:  Ann Transl Med       Date:  2021-08

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Journal:  Oxid Med Cell Longev       Date:  2021-10-27       Impact factor: 6.543

5.  Dihydroartemisinin targets fibroblast growth factor receptor 1 (FGFR1) to inhibit interleukin 17A (IL-17A)-induced hyperproliferation and inflammation of keratinocytes.

Authors:  Baojiang Chen; Chen Li; Guizhen Chang; Huan Wang
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6.  Ginsenoside Rb1 improves intestinal aging via regulating the expression of sirtuins in the intestinal epithelium and modulating the gut microbiota of mice.

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Review 7.  Immunoregulation by Artemisinin and Its Derivatives: A New Role for Old Antimalarial Drugs.

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Journal:  Front Immunol       Date:  2021-09-09       Impact factor: 7.561

  7 in total

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