Tea (Camellia sinensis) ameliorates DSS-induced colitis and liver injury by inhibiting TLR4/NF-?B/NLRP3 inflammasome in mice

文献类型： 外文期刊

第一作者： Liu, Haiyan

作者： Liu, Haiyan;Cao, Fanrong;Chen, Ruohong;Wen, Shuai;Li, Qiuhua;Lai, Xingfei;Zhang, Zhenbiao;Sun, Lingli;Sun, Shili

作者机构：

关键词： Camellia sinensis six types of tea; DSS-induced colitis; Liver injury; Gut-liver axis; NLRP3

期刊名称：BIOMEDICINE & PHARMACOTHERAPY （ 影响因子：7.419； 五年影响因子：6.581 ）

ISSN： 0753-3322

年卷期： 2023 年 158 卷

页码：

收录情况： SCI

摘要： The gut-liver axis is a bidirectional relationship between the gut with its microbiota and the hepatic. Ulcerative colitis (UC) disrupts the intestinal barrier and influx of intestinal microorganisms and their products into the liver, which trigger liver injury. Tea consumption is associated with a low incidence of UC in Asian countries. In this study, we revealed the mechanisms of six types of tea water extracts (TWEs) obtained from the leaves of Camellia sinensis on the dextran sodium sulfate (DSS)-induced colitis and liver injury in mice. The TWEs significantly restored mucin production and increased the expression levels of tight junction (TJ) proteins such as zonula occludens-1 (ZO-1), occluding, and claudin-1. In addition, TWEs also reduced the levels of pro -inflammatory cytokines in the colon and liver tissue by inactivating the NF-kappa B/NLRP3. Moreover, TEWs treat-ment promoted the integrity of the intestinal barrier to reduce serum lipopolysaccharide (LPS) levels, thereby reducing liver injury caused by intestinal microbial translocation and LPS induction. Analysis of 16 S rRNA microbial sequencing revealed that tea water extracts (TWEs) restored the DSS-induced gut dysbiosis. Interest-ingly, our results showed that the degree of fermentation of tea leaves was negatively associated with the alleviation of DSS-induced colitis effects, and there was also an overall negative trend with colitis-induced liver injury, except for black tea. Taken together, tea consumption mitigated DSS-induced colitis and liver injury in mice via inhibiting the TLR4/NF-kappa B/NLRP3 inflammasome pathway.

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