Dihydroartemisinin ameliorates dextran sulfate sodium induced inflammatory bowel diseases in mice

化学 双氢青蒿素 结肠炎 厚壁菌 小桶 实时聚合酶链反应 基因表达 促炎细胞因子 炎症 分子生物学 微生物学 基因 生物化学 免疫学 转录组 16S核糖体RNA 生物 青蒿素 疟疾 恶性疟原虫
作者
Zili Lei,Yanhong Yang,Shaomin Liu,Yuting Lei,Lanxiang Yang,Xueying Zhang,Wanwan Liu,Huijuan Wu,Changyuan Yang,Jiao Guo
出处
期刊:Bioorganic Chemistry [Elsevier BV]
卷期号:100: 103915-103915 被引量:26
标识
DOI:10.1016/j.bioorg.2020.103915
摘要

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.
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