Scandinavian journal of gastroenterology · 1997
Recombinant human transforming growth factor beta 3 accelerates gastric ulcer healing in rats.
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Coerper S, Sigloch E, Cox D, Starlinger M, Köveker G, Becker H D
Аннотация
BACKGROUND: Gastric ulcer healing is mediated by various endogenous growth factors. In this experimental study effect of locally and systemically applied recombinant human transforming growth factor beta 3 (rhTGF-beta 3) on gastric ulcer healing was investigated in the rat.
METHODS AND RESULTS: Gastric ulcers were induced with a cryoprobe, and ulcer healing was evaluated 7 days after local infiltration (0.5 micrograms, 1.0 microgram, 2.5 micrograms, and 50 micrograms) or systemic (intravenous) application of TGF-beta 3 (500 micrograms/kg body weight). Compared with controls, a dose-dependent stimulation of ulcer healing (as evidenced by a reduction in ulcer size) was observed 7 days after local infiltration of TGF-beta 3 (1.0 microgram, 2.5 micrograms, and 50 micrograms). Corresponding increases in the levels of proliferating cell nuclear antigen (PCNA) and intracellular TGF-beta 3 expression and a downregulation of the TGF-beta type-II receptor expression were also observed in the granulation tissue of the ulcer margins. Systemic application of TGF-beta 3 produced effects similar to those observed after local treatment with 50 micrograms of the compound.
CONCLUSION: Local and systemic TGF-beta 3 treatment accelerates gastric ulcer healing in rats.
METHODS AND RESULTS: Gastric ulcers were induced with a cryoprobe, and ulcer healing was evaluated 7 days after local infiltration (0.5 micrograms, 1.0 microgram, 2.5 micrograms, and 50 micrograms) or systemic (intravenous) application of TGF-beta 3 (500 micrograms/kg body weight). Compared with controls, a dose-dependent stimulation of ulcer healing (as evidenced by a reduction in ulcer size) was observed 7 days after local infiltration of TGF-beta 3 (1.0 microgram, 2.5 micrograms, and 50 micrograms). Corresponding increases in the levels of proliferating cell nuclear antigen (PCNA) and intracellular TGF-beta 3 expression and a downregulation of the TGF-beta type-II receptor expression were also observed in the granulation tissue of the ulcer margins. Systemic application of TGF-beta 3 produced effects similar to those observed after local treatment with 50 micrograms of the compound.
CONCLUSION: Local and systemic TGF-beta 3 treatment accelerates gastric ulcer healing in rats.