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1

Plasma citrulline level as a biomarker for cancer therapy-induced small bowel mucosal damage

100%
Barzal J. A., Szczylik C., Rzepecki P., Jaworska M., Anuszewska E.
Acta Biochimica Polonica
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2014
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tom 61
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nr 4
2
Content available remote

Hierarchies of healing in gut mucosal injury

100%
Basson M. D.
Journal of Physiology and Pharmacology
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2017
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tom 68
|
nr 6
3
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Direct protective action of epidermal growth factor on isolated gastric mucosal surface epithelial cells

100%
Ishikawa T., Fukuda T., Sugiyama M., Tarnawski A.
Journal of Physiology and Pharmacology
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1992
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tom 43
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nr 4
Epidermal growth factor (EGF) protects gastric mucosa against acute injury produced by a variety of damaging agents, but the mechanism of its protective action is not clear. Since the surface epithelial cells (SEC) are important component of gastric mucosal defence, we studied whether EGF may directly protect isolated gastric SEC against ethanol injury in vitro, in condition independent of systemic factors and whether endogenous prostaglandins may play a role in EGF’s protective action. The isolated SEC from rat gastric mucosa were preincubated in medium only, or medium containing 0.0001-10.0 µg/ml of h-rEGF for 15 minutes, and incubated with 8% ethanol for 1 hour. In another study the above experiment was repeated but cells were pretreated with 10⁻⁴ or 10⁻⁵ M indomethacin before EGF treatment. The cell viability was assessed by fast green exclusion test. Incubation of SEC with 8% ethanol significantly reduced SEC cell viability to 50 ₋⁺ 2%: EGF 0.1 or 1.0/µg/ml significantly reduced ethanol induced damage (cell viability 59 ₋⁺ 3 and 62₋⁺ 3% respectively). Pretreatment with 10⁻⁴ M indomethacin (the dose which does not affect SEC viability but inhibit PGE₂ and PGI₂ generation), significantly reduced protective action of EGF against 8% ethanol injury. EGF 1.0 and 10.0 µg/ml alone without ethanol increased PGE₂ and 6 keto PGF₁α generation by SEC. These studies demonstrated: 1) EGF is able to protect gastric surface epithelial cells directly without mediation by systemic factors. 2) EGF induced protection of SEC may in part be mediated by prostaglandins.
4
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Neural aspects of ghrelin-induced gastroprotection against mucosal injury induced by noxious agents

80%
Brzozowski T., Konturek P. C., Sliwowski Z., Drozdowicz D., Kwiecien S., Pawlik M., Pajdo R., Konturek S. J., Pawlik W. W., Hahn E. G.
Journal of Physiology and Pharmacology. Supplement
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2006
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tom 57
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nr 6
63-76
Ghrelin, identified in oxyntic mucosa has been recently implicated in the control of food intake and growth hormone (GH) release but whether this hormone can influence the gastric secretion and gastric mucosal integrity have been little studied. We compared the effects of intraperitoneal (i.p.) and intracerebroventricular (i.c.v.) administration of ghrelin on gastric secretion in rats equipped with gastric fistula (GF) and gastric lesions induced in rats by 75% ethanol and ischemia-reperfusion (I/R) with or without vagotomy or functional ablation of afferent sensory nerves by capsaicin. The number and the area of gastric lesions was measured by planimetry, the GBF was assessed by H2-gas clearance method and blood was withdrawn for the determination of the plasma ghrelin and gastrin levels. Ghrelin (5-80 µg/kg i.p. or 600-5000 ng/rat i.c.v.) increased gastric acid secretion and attenuated gastric lesions induced by ethanol and I/R. These protective effects of ghrelin were accompanied by the significant rise in the gastric mucosal blood flow (GBF) and plasma ghrelin and gastrin levels. Ghrelin given i.p. or injected i.c.v. in standard doses 20 µg/kg or 5000 ng/kg, respectively, significantly attenuated the gastric mucosal damage and significantly raised the GBF. Ethanol applied i.g. in smaller concentrations (12.5% and 25%) produced a significant increase in plasma immunorective ghrelin levels and this effect was inhibited in rats receiving ethanol in higher concentrations (75% and 100%). Ghrelin-induced protection after its i.p. or i.c.v. administration and accompanying increase in the GBF were completely abolished by vagotomy and capsaicin-deactivation of sensory nerves. Concurrent treatment with CGRP added to ghrelin restored the gastroprotective and hyperemic effects of ghrelin applied i.p. or i.c.v. in rats with capsaicin denervation. We conclude that central and peripheral ghrelin exerts a potent protective and gastric secretory effects in rats exposed to ethanol and I/R, and that these actions involve vagal nerve integrity, partially depending upon afferent nerves and hyperemia mediated by sensory neuropeptides such as CGRP released from these nerves.
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