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Effect of resveratrol on Treg/Th17 signaling and ulcerative colitis treatment in mice.

AbstractAIM:
To determine the therapeutic efficacy of resveratrol on ulcerative colitis (UC) and its underlying mechanisms.
METHODS:
The mouse UC model was developed using 5% dextran sulfate sodium. Mice were randomly divided into four groups: normal control, UC model group, resveratrol low-dose group (RLD; 50 mg/kg per day), and resveratrol high-dose group (RHD; 100 mg/kg per day).
RESULTS:
The results showed that RLD regulates Treg/Th17 balance mainly through reducing the number of Th17 cells, whereas RHD regulates Treg/Th17 balance through both downregulating the number of Th17 cells and upregulating the number of Treg cells. Resveratrol can also regulate the level of plasma and intestinal mucosal cytokines including interleukin (IL)-10, transforming growth factor-β1, IL-6, and IL-17. The expressions of hypoxia inducible factor (HIF)-1α, mammalian target of rapamycin (mTOR), and signal transducer and activator of transcription 3 were significantly decreased in the intestinal tissues of mice treated with resveratrol.
CONCLUSION:
The therapeutic efficacy of resveratrol in UC is dose dependent and closely associated with the regulation of Treg/Th17 balance and the HIF-1α/mTOR signaling pathway.
AuthorsJun Yao, Cheng Wei, Jian-Yao Wang, Ru Zhang, Ying-Xue Li, Li-Sheng Wang
JournalWorld journal of gastroenterology (World J Gastroenterol) Vol. 21 Issue 21 Pg. 6572-81 (Jun 07 2015) ISSN: 2219-2840 [Electronic] United States
PMID26074695 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Cytokines
  • Hif1a protein, mouse
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Inflammation Mediators
  • STAT3 Transcription Factor
  • Stat3 protein, mouse
  • Stilbenes
  • Dextran Sulfate
  • mTOR protein, mouse
  • TOR Serine-Threonine Kinases
  • Resveratrol
Topics
  • Animals
  • Colitis (chemically induced, immunology, metabolism, pathology, prevention & control)
  • Colon (drug effects, immunology, metabolism, pathology)
  • Cytokines (metabolism)
  • Dextran Sulfate
  • Disease Models, Animal
  • Dose-Response Relationship, Drug
  • Hypoxia-Inducible Factor 1, alpha Subunit (metabolism)
  • Inflammation Mediators (metabolism)
  • Male
  • Mice, Inbred BALB C
  • Resveratrol
  • STAT3 Transcription Factor (metabolism)
  • Signal Transduction (drug effects)
  • Spleen (drug effects, immunology, metabolism)
  • Stilbenes (pharmacology)
  • T-Lymphocytes, Regulatory (drug effects, immunology, metabolism)
  • TOR Serine-Threonine Kinases (metabolism)
  • Th17 Cells (drug effects, immunology, metabolism)
  • Time Factors

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