Background/aims: Growth factors have a potential role in gastrointestinal mucosal repair. Although basic fibroblast growth factor (bFGF) is known to contribute to wound healing, however, the role of bFGF in the treatment of inflammatory bowel disease has not been established. The aim of this study is to investigate the therapeutic effects of intracolonic bFGF administration on both the clinical symptoms and histological mucosal repair in an experimental model of colitis in rats.
Methodology: Acute colitis was induced with 5% dextran sulfate sodium (DSS) given for one week in drinking water. The rats were treated daily with recombinant human bFGF enema (400 microg/kg/day) or vehicle once daily from day 1 to day 7. Clinical score (stool consistency, weight loss and hemoccult/gross rectal bleeding), colon length and histological score of mucosal injury in colonic tissue samples were analyzed.
Results: Administration of bFGF enema significantly reduced clinical score (p < 0.01) and histological score (p < 0.01). No specific side effect of bFGF was noted.
Conclusions: These results suggest that bFGF enema is clinically safe and useful in the treatment of inflammatory bowel disease. BFGF enema may contribute as a novel therapy of IBD.
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J Physiol Pharmacol
October 2015
Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
Previously, we reported that TGP-580, a mutein of human basic fibroblast growth factor (bFGF), accelerated the healing of gastric and duodenal ulcers in rats. In the present study, we examined the effect of TGP-580 on the healing of colonic ulcers. In male Sprague Dawley rats, ulcers were induced in the colon 6 cm from the anus by enema of 50 μl of 3% N-ethylmaleimide, a sulfhydryl alkylator.
View Article and Find Full Text PDFCurr Pharm Des
March 2016
Department of Pathology, SOM, University of California, Irvine, CA, USA.
Ulcers in the stomach, duodenum, ileum/jejunum and colon may look alike grossly and microscopically, but they have very different etiologies and pathogenesis. Unfortunately, there is virtually no etiologic treatment for any of these lesions which are also accompanied by limited or extensive inflammation. This article reviews four groups of new antiulcer drugs discovered and patented in our lab in Boston and Long Beach/Irvine (Table 1).
View Article and Find Full Text PDFJ Pharmacol Exp Ther
November 2011
Diagnostic and Molecular Medicine Health Care Group, VA Long Beach Healthcare System, Long Beach, CA 90822, USA.
We demonstrated previously that basic fibroblast growth factor (bFGF) accelerated the healing of experimental duodenal ulcers, and we now hypothesize that bFGF might also accelerate the healing of experimental ulcerative colitis (UC). We also explored the potential molecular mechanisms involved in the accelerated healing of UC in rats treated with bFGF. The results demonstrated that colonic lesions were significantly reduced by bFGF treatment, whereas neutralization of bFGF aggravated iodoacetamide-induced UC.
View Article and Find Full Text PDFCurr Pharm Des
November 2011
Diagnostic and Molecular Medicine Health Care Group, Veterans Affairs Medical Center and Departments of Pathology, Pharmacology and Medicine, University of California, Irvine, School of Medicine, Long Beach, California 90822, USA.
Gastrointestinal (GI) ulcers are essentially internal wounds that resist normal healing processes. Since their pathogenesis is poorly understood, and the etiologic (e.g.
View Article and Find Full Text PDFHepatogastroenterology
December 2007
Department of Surgical Oncology, University of Tokyo Graduate School of Medicine, Japan.
Background/aims: Growth factors have a potential role in gastrointestinal mucosal repair. Although basic fibroblast growth factor (bFGF) is known to contribute to wound healing, however, the role of bFGF in the treatment of inflammatory bowel disease has not been established. The aim of this study is to investigate the therapeutic effects of intracolonic bFGF administration on both the clinical symptoms and histological mucosal repair in an experimental model of colitis in rats.
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