Korean J Gastroenterol.  2000 Jun;35(6):755-769.

Modulation of Intestinal Inflammation by Fibroblast Growth Factor-10 in Indomethacin-Induced Small Intestinal Ulceration in Rats

Abstract

BACKGROUND/AIMS
Fibroblast growth factor-10 (FGF-10) is a homolog of keratinocyte growth factor-2 with epithelial mitogenic activity. We investigated the therapeutic role of FGF-10 in intestinal ulceration and its mechanism of protection.
METHODS
FGF-10 was administered before or after induction of small intestinal ulceration by indomethacin. FGF-10 was injected subcutaneously (1 or 5 mg/kg) and intravenously (1 mg/kg) daily for 6 days (acute study). Injury was evaluated by double-blinded macroscopic and microscopic scores, and the concentration of tissue interleukin (IL)-1beta and the expression of collagen type I RNA were compared. It was determined whether FGF-10 has an effect on in vitro epithelial cellular proliferation, restitution of wounded monolayers, the expression of cyclooxygenase-2 (COX-2) and collagen, and regulation of NF-KB.
RESULTS
Intravenous FGF-10 significantly decreased acute intestinal injury by all parameters. FGF-10 promoted in vitro proliferation and migration of epithelial cell, and stimulated COX-2 expression, but had no effect on IKB degradation. FGF-10 affected up-regulated collagen expression in cultured myofibroblasts but not in vivo fibrosis.
CONCLUSIONS
FGF-10 treats intestinal inflammation by actively promoting the mechanism to heal epithelial cells.

Keyword

Fibroblast growth factor-10; Intestinal inflammation; Restitution; Prostaglandin

MeSH Terms

Animals
Cell Proliferation
Collagen
Collagen Type I
Cyclooxygenase 2
Epithelial Cells
Fibroblasts*
Fibrosis
Indomethacin
Inflammation*
Interleukins
Keratinocytes
Myofibroblasts
NF-kappa B
Rats*
RNA
Ulcer*
Wounds and Injuries
Collagen
Collagen Type I
Cyclooxygenase 2
Indomethacin
Interleukins
NF-kappa B
RNA
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