The aim of our study was to evaluate the role of the epidermal growth factor (EGF), interleukin-1 (IL-1) and of lipid peroxides (TBARS) in the development and healing of experimental gastric ulcer in the rat. In 66 male Sprague Dowley rats, gastric ulcer was induced by means of the serosal application of 100% acetic acid. The animals were followed up for 1 (6 cases), 3 (6) and 5 (6) hours, and 1 (6 cases), 2 (6), 3 (7), 5 (6), 10 (6) 15 (6) and 21 (6) days. Five animals were sham operated. Samples from the ulcer margin (U), from an ulcer adjacent area (UAA) and from the antrum (A) were obtained. All treated animals developed gastric ulcer, evident just after one hour; the ulcer progressively healed and after 21 days all were scarred. Mucosal U-EGF significantly increased immediately after ulcer induction; it progressively and slowly decreased paralleling ulcer scarring. UAA-EGF and A-EGF behaved likewise: they significantly increased after 1, 3 and 5 hours and returned to normal levels just 1 day after ulcer induction. Variations in mucosal IL-1 were similar to those in EGF, a correlation being found between these two parameters. The EGF serum levels of rats with ulcers of 1 and 5 hours, were significantly lower than those of controls. One day after ulcer induction, U-TBARS levels were increased, and the high levels persisted, even when the ulcers had healed. In conclusion: (1) the rapid increase in mucosal EGF occurring in the presence of gastric ulcer may be consequent to an enhanced local and/or submandibular production; (2) the parallel behaviour between EGF and IL-1 suggests that this cytokine may play a role in stimulating EGF production; (3) chronic gastric ulcer is associated with an enhancement of lipid peroxidation phenomena, which persist after healing and which may create a "loci minoris resistentiae". © 1995.

Role of epidermal growth factor, interleukin-1 and lipid peroxidation in healing of experimental gastric ulcer in rats / Plebani, Mario; Battistel, Marzia; Basso, Daniela; Panozzo, Maria Piera; Cavallini, Letizia; Metus, Paolo; Di Mario, Francesco; Cecchetto, Attilio. - In: PATHOPHYSIOLOGY. - ISSN 0928-4680. - 2:2(1995), pp. 103-108. [10.1016/0928-4680(95)00014-R]

Role of epidermal growth factor, interleukin-1 and lipid peroxidation in healing of experimental gastric ulcer in rats

Di Mario, Francesco;
1995

Abstract

The aim of our study was to evaluate the role of the epidermal growth factor (EGF), interleukin-1 (IL-1) and of lipid peroxides (TBARS) in the development and healing of experimental gastric ulcer in the rat. In 66 male Sprague Dowley rats, gastric ulcer was induced by means of the serosal application of 100% acetic acid. The animals were followed up for 1 (6 cases), 3 (6) and 5 (6) hours, and 1 (6 cases), 2 (6), 3 (7), 5 (6), 10 (6) 15 (6) and 21 (6) days. Five animals were sham operated. Samples from the ulcer margin (U), from an ulcer adjacent area (UAA) and from the antrum (A) were obtained. All treated animals developed gastric ulcer, evident just after one hour; the ulcer progressively healed and after 21 days all were scarred. Mucosal U-EGF significantly increased immediately after ulcer induction; it progressively and slowly decreased paralleling ulcer scarring. UAA-EGF and A-EGF behaved likewise: they significantly increased after 1, 3 and 5 hours and returned to normal levels just 1 day after ulcer induction. Variations in mucosal IL-1 were similar to those in EGF, a correlation being found between these two parameters. The EGF serum levels of rats with ulcers of 1 and 5 hours, were significantly lower than those of controls. One day after ulcer induction, U-TBARS levels were increased, and the high levels persisted, even when the ulcers had healed. In conclusion: (1) the rapid increase in mucosal EGF occurring in the presence of gastric ulcer may be consequent to an enhanced local and/or submandibular production; (2) the parallel behaviour between EGF and IL-1 suggests that this cytokine may play a role in stimulating EGF production; (3) chronic gastric ulcer is associated with an enhancement of lipid peroxidation phenomena, which persist after healing and which may create a "loci minoris resistentiae". © 1995.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11381/2844295
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