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Published on: September 12, 2019
Therapeutic effects of rectal administration of basic fibroblast growth factor on experimental murine colitis
Minoru Matsuura1, Kazuichi Okazaki, Akiyoshi Nishio
1Department of Gastroenterology and Endoscopic Medicine, Kyoto University, Kyoto, Japan.
Background & Aims:
Basic fibroblast growth factor (bFGF) is a promising therapeutic agent for various diseases. It remains unclear, however, whether bFGF is effective for the treatment of inflammatory bowel disease. The aim of this study was to examine the efficacy of bFGF on 2 experimental murine colitis models and to investigate its molecular mechanisms.
Methods:
We evaluated the effects of human recombinant bFGF (hrbFGF) on mice with dextran sulfate sodium (DSS)-induced colitis and mice with trinitrobenzene sulfonic acid (TNBS)-induced colitis as well as normal mice. Body weight, survival rate, and histologic findings of the colonic tissues were examined. Gene expression of tumor necrosis factor (TNF)-alpha, cyclooxygenase (COX)-2, transforming growth factor (TGF)-beta, mucin 2 (MUC2), intestinal trefoil factor (ITF), and vascular endothelial growth factor (VEGF) in the colonic tissues was determined. The proliferation activity of hrbFGF on the colonic epithelium was evaluated by immunohistochemistry.
Results:
Rectal administration of hrbFGF ameliorated DSS-induced colitis in a dose-dependent manner. Gene expression of TNF-alpha was significantly reduced in the colonic tissues of mice with DSS-induced colitis treated with hrbFGF, whereas MUC2 and ITF messenger RNA expression was up-regulated. Rectal administration of hrbFGF significantly improved the survival rate of mice with TNBS-induced colitis and partially ameliorated colitis. hrbFGF significantly increased the number of Ki-67-positive cells in the colonic epithelium of normal mice, and up-regulated the gene expression of COX-2, TGF-beta, MUC2, ITF, and VEGF in the colonic tissues.
Conclusions:
Rectal administration of bFGF might be a promising option for the treatment of inflammatory bowel disease.
Insights
Basic fibroblast growth factor (bFGF) shows promise for treating inflammatory bowel disease. Rectal bFGF administration improved colitis in mouse models by reducing inflammation and promoting healing.
Area of Science:
- Gastroenterology
- Molecular Biology
- Regenerative Medicine
Background:
- Basic fibroblast growth factor (bFGF) is a potential therapeutic agent for various conditions.
- Its efficacy in treating inflammatory bowel disease (IBD) remains largely unexplored.
- This study investigates bFGF's therapeutic potential in experimental colitis models.
Purpose of the Study:
- To evaluate the efficacy of basic fibroblast growth factor (bFGF) in dextran sulfate sodium (DSS)-induced and trinitrobenzene sulfonic acid (TNBS)-induced murine colitis models.
- To elucidate the molecular mechanisms underlying bFGF's effects on colitis.
Main Methods:
- Human recombinant bFGF (hrbFGF) was administered rectally to mice with DSS- and TNBS-induced colitis.
- Evaluated outcomes included body weight, survival rates, and colonic tissue histology.
- Assessed gene expression of key inflammatory and regenerative markers (TNF-alpha, COX-2, TGF-beta, MUC2, ITF, VEGF) and epithelial proliferation (Ki-67).
Main Results:
- hrbFGF ameliorated DSS-induced colitis dose-dependently, reducing TNF-alpha and increasing MUC2 and ITF expression.
- hrbFGF improved survival and partially alleviated TNBS-induced colitis.
- In normal mice, hrbFGF increased colonic epithelial proliferation and upregulated expression of COX-2, TGF-beta, MUC2, ITF, and VEGF.
Conclusions:
- Rectal administration of bFGF demonstrates therapeutic potential for inflammatory bowel disease.
- bFGF may exert its effects by modulating inflammatory responses and promoting tissue repair and regeneration.
