Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver · 2003
Effect of exogenous administration of transforming growth factor-beta and famotidine on the healing of duodenal ulcer under the impact of indomethacin.
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Pérez-Aisa A, Sopeña F, Arceiz E, Ortego J, Sainz R, Lanas A
Аннотация
BACKGROUND: Non-steroidal anti-inflammatory drugs delay ulcer healing and cause refractory peptic ulcers in humans.
OBJECTIVE: To study the effects of growth factors on experimental duodenal ulcer healing in indomethacin-treated rats.
METHODS: Duodenal ulcers were induced in male Wistar rats by the serosal application of 75% acetic acid for 10 s. Rats were then treated with indomethacin (2 mg/kg/day; s.c.), transforming growth factor beta (15 ng locally injected subserosally at the ulcer site) or famotidine (5 mg/kg/day; p.o.), vehicle or combinations of treatments. On day 5, 8 or 12, rats were sacrificed and the ulcer area planimetrically measured under a dissecting microscope. Macroscopic area, microscopic diameter, collagen content and mucosal regeneration were assessed in histological preparations. Gastric secretion was assessed also in the pylorus-ligated rat-model. Data expressed as median and ranges were analyzed by non-parametric test.
RESULTS: Indomethacin delayed ulcer healing but transforming growth factor-beta and famotidine improved ulcer healing and reversed the effects of indomethacin. Maximal differences were observed on day 8. Transforming growth factor-beta was associated with an increase in epithelial and granulation tissue cell proliferation. Famotidine induced a profound inhibition of gastric secretion and increased collagen secretion but it did not affect cell proliferation.
CONCLUSIONS: Transforming growth factor-beta and famotidine accelerate ulcer healing delayed by indomethacin.
OBJECTIVE: To study the effects of growth factors on experimental duodenal ulcer healing in indomethacin-treated rats.
METHODS: Duodenal ulcers were induced in male Wistar rats by the serosal application of 75% acetic acid for 10 s. Rats were then treated with indomethacin (2 mg/kg/day; s.c.), transforming growth factor beta (15 ng locally injected subserosally at the ulcer site) or famotidine (5 mg/kg/day; p.o.), vehicle or combinations of treatments. On day 5, 8 or 12, rats were sacrificed and the ulcer area planimetrically measured under a dissecting microscope. Macroscopic area, microscopic diameter, collagen content and mucosal regeneration were assessed in histological preparations. Gastric secretion was assessed also in the pylorus-ligated rat-model. Data expressed as median and ranges were analyzed by non-parametric test.
RESULTS: Indomethacin delayed ulcer healing but transforming growth factor-beta and famotidine improved ulcer healing and reversed the effects of indomethacin. Maximal differences were observed on day 8. Transforming growth factor-beta was associated with an increase in epithelial and granulation tissue cell proliferation. Famotidine induced a profound inhibition of gastric secretion and increased collagen secretion but it did not affect cell proliferation.
CONCLUSIONS: Transforming growth factor-beta and famotidine accelerate ulcer healing delayed by indomethacin.