Camellia sinensis and Litsea coreana Ameliorate Intestinal Inflammation and Modulate Gut Microbiota in Dextran Sulfate Sodium‐Induced Colitis Mice

Scope Polyphenol‐enriched herbal extracts have been proved as alternative therapeutic strategies for experimentally induced colitis. The in vivo and in vitro anti‐inflammatory effects of Camellia sinensis (green, white, yellow, oolong, black, and dark tea) and Litsea coreana (hawk tea) are comparatively explored. Methods and results HPLC analysis confirms dissimilarities among phytochemical compositions of these teas. The tea extracts (TEs) significantly decrease the production of pro‐inflammatory cytokines (IL‐6, IL‐12, and tumor necrosis factor‐α) and increase the anti‐inflammatory cytokines (IL‐10) in LPS‐stimulated RAW 264.7 macrophages and a dextran sodium sulfate (DSS)‐induced colitis mouse model. The treatment of TEs in colitis mice can ameliorate colon inflammation, pro‐oxidative enzyme activity, colon integrity, and suppress the activation of nuclear factor‐κB. Of note, green TE significantly attenuates the DSS‐induced decrease in richness and diversity of gut microbiota. Moreover, TEs are capable of exerting a prebiotic effect on gut microbiota by increasing the abundance of potentially beneficial bacteria (e.g., Faecalibaculum, and Bifidobacterium), and decreasing the abundance of potentially harmful bacteria (e.g., Bacteroids, and Mucispirillum). TEs restore the decreased production of SCFAs in the feces of colitic mice. Conclusion The treatment of seven types of tea can alleviate DSS‐induced colitis in mice, and modulate the dysbiosis of gut microbiota in colitis mice. Camellia sinensis and Litsea coreana ameliorate can modulate colon inflammation, pro‐oxidative enzyme activity, damage of colon integrity, and activation of nuclear factor‐kappa B. They also modulate dextran sodium sulfate‐induced gut microbiota dysbiosis by increasing potentially beneficial bacteria and decreasing potentially harmful bacteria, and restore the decreased production of short‐chain fatty acids in the feces of colitic mice.