Highlights
(1) TGs inhibits intestinal inflammation by down-regulating the expression of NF-κB and JAK2.
(2) TGs can effectively alleviate intestinal damage caused by IBD disease.
(3) TGs can restore intestinal homeostasis in diseased mice.
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(1) TGs inhibits intestinal inflammation by down-regulating the expression of NF-κB and JAK2.
(2) TGs can effectively alleviate intestinal damage caused by IBD disease.
(3) TGs can restore intestinal homeostasis in diseased mice.
This study investigates the protective effects of total glycosides of Cistanche (TGs) on the intestinal tract of inflammatory bowel disease (IBD) mice induced by dextran sulfate sodium (DSS) from the perspectives of immune regulation and intestinal homeosta. We evaluated the IBD disease activity index (DAI) and histopathological changes of the colon tissue in mice, and validated the involvement of NF-κB and JAK2 in TGS-mediated IBD regulation by real-time quantitative PCR (qRT-PCR), serum enzyme-linked immunosorbent assay (ELISA), and TUNEL Cell Apoptosis Detection. Finally, we analyzed the changes in the intestinal microbiome. The results show that TGs can effectively improve the disease activity index of sick mice, alleviate the damage to the epithelial barrier, improve the morphology of the intestinal epithelial tissue, and reduce the infiltration of inflammatory cells in the damaged colon. TGs inhibit the activation of the two key signal targets of NF-κB and JAK2, reduce the expression of inflammatory factors such as IL-1 and TNF-α, and increase the expression of anti-inflammatory factor IL-10. In addition, TGs reduce the abundance of Proteobacteria, increase the proportion of Bacteroidetes and Thermotogae, and upregulate the numbers of Bacteroides, Lachnospiraceae_NK4A136_group, and Oscillospiraceae to alleviate intestinal microbiome dysbiosis and restore intestinal microenvironmental homeosta. In summary, these research results suggest that TGs can improve IBD by alleviating inflammation and restoring intestinal homeosta, providing experimental evidence for the mechanism of Cistanche intervention in IBD.
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