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Exploring the Role of Inulin in Targeting the Gut Microbiota: An Innovative Strategy for Alleviating Colonic Fibrosis
Kaihua Ji1, Manman Zhang1, Liqing Du1
1Tianjin Key Laboratory of Radiation Medicine and Molecular Nuclear Medicine, Department of Radiobiology, Institute of Radiation Medicine of Chinese Academy of Medical Science & Peking Union Medical College, State Key Laboratory of Advanced Medical Materials and Devices, Tianjin 300192, PR China.
Inulin supplements protect against radiation-induced colonic fibrosis by promoting beneficial gut bacteria that produce short-chain fatty acids (SCFAs). These SCFAs and their metabolites reduce fibrosis markers in cell and mouse models.
Area of Science:
- Gastroenterology
- Oncology
- Microbiology
Background:
- Radiation therapy for pelvic and abdominal cancers can cause radiation enteropathy.
- Chronic colonic fibrosis is a common gastrointestinal complication of radiation therapy.
Purpose of the Study:
- To investigate the efficacy of inulin supplements in preventing radiation-induced colonic fibrosis.
- To explore the role of gut microbiota and short-chain fatty acids (SCFAs) in this protective effect.
Main Methods:
- Administered inulin supplements to mice undergoing irradiation.
- Transplanted gut microbiota and fecal metabolites from inulin-treated mice into a mouse model of radiation enteropathy.
- Assessed gene expression related to fibrosis and extracellular matrix synthesis in NIH/3T3 cells treated with inulin-derived metabolites.
Main Results:
- Inulin supplementation reduced colonic fibrosis in a mouse model.
- Transplantation of microbiota and metabolites from inulin-treated mice ameliorated colonic fibrosis.
- Inulin-derived metabolites significantly decreased the expression of fibrosis-related genes and collagen production in NIH/3T3 cells.
- These metabolites also suppressed genes involved in the extracellular matrix synthesis pathway.
Conclusions:
- Inulin shows promise as a protective agent against radiation-induced colonic fibrosis.
- The mechanism involves modulation of gut microbiota, SCFA production, and subsequent reduction in fibrotic pathways.
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