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- Title
茯砖茶对葡聚糖硫酸钠诱导UC小鼠炎症 及肠道微生物的影响.
- Authors
黄翔翔; 谭婷; 禹利君; 王坤波; 黄建安; 徐诗飪; 刘仲华
- Abstract
In this study, we investigated the effects of Fu brick tea on the anti-inflammation and intestinal microflora of ulcerative colitis (UC) mice induced by Dextran sulfate sodium (DSS). Sixty C57BL/6 female mice were randomly divided into the normal control group, 10 mg kg1 EGCG control group, high dose brick tea (300 mg-kg1, HBT) control group, DSS model group, DSS+ 10 mg kg1 EGCG group, DSS + low dose brick tea (100 mg kg1, LBT) group, DSS+middle dose brick tea (150 mg kg_1' MBT) group and DSS+HBT group, with the control groups n=5 and the treatment groups n=9. After 1 week of DSS modeling, the mice were gavaged for 4 weeks. The mice were executed after 5 weeks of the treatments. The histopathological changes of mice colon were observed, and the disease activity index (DAI) of mice colitis was assessed. The levels of IL-6-IL-8-IL・1尻 TNF-a and IFN-y inflammatory factors in mice serum and the expression levels of JAK2 and STAT3 genes in mice colon tissues were measured. The intestinal microflora of mice was analyzed by PCR-DGGE and clone sequencing techniques. The results show that compared with the DSS model group, the quality of survival and colonic tissue morphology of mice were significantly improved after feeding EGCG and different concentrations of brick tea, and the levels of inflammatory factors IL-6, IL-8, IL・1尻 TNF-a and IFN-y in mice serum were significantly reduced (P<0.05). Moreover, the expressions of JAK2 and STAT3 genes were significantly reduced (P<0.05) JAK2/STAT3 inflammatory signaling pathway was inhibited; and intestinal microflora diversity and richness were increased significantly. The dominant bacterial flora in different treatment groups were changed as well. In conclusion, Fu brick tea can ameliorate DSS-induced UC injury by inhibiting JAK2ISTAT3 inflammatory signaling pathway and modulating intestinal microflora diversity.
- Publication
Journal of Tea Science, 2021, Vol 41, Issue 5, p681
- ISSN
1000-369X
- Publication type
Article