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Research Article | Open Access

Total Glycosides of Cistanche deserticola attenuates DSS-induced inflammatory bowel disease by regulating intestinal environmental homeostasis

Shao-shi Zhang1,2Duo Feng1,2Jian-zhang An1,2Jian Zhao1,2Jiang-yan Zhao1,2Yu Guo1,2Yong-jun Jiang3Wen-jie Yan1,2( )
Beijing Key Laboratory of Bioactive Substances and Functional Food, College of Biochemical Engineering, Beijing Union University, Beijing 100191, China
College ofBiochemical Engineering, Beijing Union University, Beijing 100023, China
Inner Mongolia Sankou Biotechnology Co., LTD., Ordos 017000, Inner Mongolia, China
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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.

Graphical Abstract

This study focused on total cistanche glycosides (TGs), the main active ingredient extracted from desert cistanche, to explore its potential application in the treatment of inflammatory bowel disease (IBD). In a DSS induced inflammatory bowel disease (IBD) mouse model, TGs demonstrated effective inhibition of NF-κB and JAK2, key molecules in the inflammatory signaling pathway, thereby regulating the expression pattern of inflammatory factors and significantly improving the abnormal apoptosis of intestinal epithelial cells. At the same time, TGs also effectively improved the imbalance of intestinal flora in IBD mice and restored the intestinal environmental balance. These findings suggest that TGs has the synergistic potential to improve IBD by reducing inflammatory responses and restoring environmental balance in the gut. This study reveals the unique advantages and broad prospects of TGs as a natural food and drug homologous resource with low toxicity and multi-pathway regulation ability in the intervention of IBD.

Abstract

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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Food & Medicine Homology
Article number: 9420048
Cite this article:
Zhang S-s, Feng D, An J-z, et al. Total Glycosides of Cistanche deserticola attenuates DSS-induced inflammatory bowel disease by regulating intestinal environmental homeostasis. Food & Medicine Homology, 2025, 2(2): 9420048. https://doi.org/10.26599/FMH.2025.9420048

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Received: 02 May 2024
Revised: 16 July 2024
Accepted: 16 July 2024
Published: 10 October 2024
© National R & D Center for Edible Fungus Processing Technology 2024. Published by Tsinghua University Press.

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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