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1
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Gastric mucosal protection: from the periphery to the central nervous system

100%
Gyires K., Toth V. E., Zadori Z. S.
Journal of Physiology and Pharmacology
|
2015
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tom 66
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nr 3
2
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Role of mucus in gastric mucosal protection

84%
Slomiany B. L., Slomiany A.
Journal of Physiology and Pharmacology
|
1991
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tom 42
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nr 2
Even though there is no general agreement as to the mechanism of gastric mucosal protection, the consensus is that the initial brunt of luminal insults falls on the mucus layer which constitutes the only identifiable physical barrier between the gastric lumen and the mucosal surface. The continuous renewal and resilient nature of this layer efficiently counters peptic erosion of the gel, assures its viscoelastic and permselective properties, and provides a milieu for containment of the diffusing luminal acid by mucosal bicarbonate. Disturbances in this delicate balance lead to the impairment of the protective function of mucus resulting in gastric disease. Indeed, the weakening of gastric mucosal defense is intimately associated with the diminished viscoelastic qualities of mucus, decrease in hydrogen ion retardation capacity, and the extensive proteolysis of its mucin component. Although until recently the disintegration of the mucus coat was attributed exclusively to the enhanced activity of intragastric pepsin, our studies provided strong argument that a bacterial factor, namely infection by Helicobacter pylori, through the action of its protease and. lipase enzymes also is highly detrimental to the integrity of gastric mucus. Hence, agents capable of interfering with the pathogenic activity of this bacteria are becoming the drugs of choice in peptic ulcer therapy.
3
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Enhancement of the physicochemical qualities of gastric mucus by sofalcone

84%
Piotrowski J., Yamaki K., Tamura S., Slomiany A., Slomiany B. L.
Journal of Physiology and Pharmacology
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1991
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tom 42
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nr 3
The effect of prolonged administration of an antiulcer drug, sofalcone, on the physicochemical properties of gastric mucus was investigated. The experiments were conducted with groups of rats receiving twice daily for three consecutive days a dose of 100 mg/kg sofalcone, while the control group received daily doses of vehicle. The rats were sacrificed 16 h after the last dose and gastric mucosa subjected to physicochemical measurements. The results revealed that sofalcone evoked a 23% increase in mucus gel dimension, while sulfo- and sialomucins content of the gel increased by 54 and 25%, respectively. These changes were accompanied by a 16% increase in mucus H⁺ retardation capacity, 2-fold increase in viscosity, and a 39% increase in the gel hydrophobicity. The mucus elaborated in the presence of sofalcone contained 67 % more covalently bound fatty acids, exhibited 10% lower content of protein, 30% higher content of carbohydrate, and 18% higher content of lipids. The mucus of the sofalcone group also showed an increase in the proportion of the high molecular weight mucus glycoprotein form, which in the control group accounted for about 30% of gel mucin, while its content in mucus gel of animals receiving sofalcone reached the value of 50%. The results indicate that sofalcone enhances the protective qualities of mucus component of gastric mucosal barrier.
4
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Leukotrienes in mucosal damage and protection

84%
Peskar B. M.
Journal of Physiology and Pharmacology
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1991
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tom 42
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nr 2
Exposure of the rat gastric mucosa to ethanol stimulates the generation of leukotriene (LTC₄) and 15-hydroxyeicosatetraenoic acid, hut not of thromboxanes and prostaglandins. Lipoxygenase activation is not found with other topical irritants or nonsteroidal anti-inflammatory drugs. A number of gastroprotective drugs dose-dependently inhibit the stimulatory action of ethanol on mucosal LTC₄ formation closely parallel to their protective activity suggesting that ethanol-induced damage and activation of lipoxygenases may involve common targets which are simultaneously counteracted by certain types of protective agents. Selective inhibition of 5-lip- oxygenase, however, does not confer protection against gastric mucosal damage caused by topical irritants or non-steroidal anti-inflammatory drugs. Thus, although leukotrienes may mediate certain reactions elicited by gastric ulcerogens such as submucosal venular constriction and mucosal micro vascular engorgement, they do not appear to be major mediators of ulcerogen-induced tissue necrosis. The contribution of other products of the various pathways of arachidonic acid metabolism to gastric mucosal injury and the mechanism underlying the close interrelationship between protection and inhibiton of LTC₄ formation observed with certain compounds remains to be investigated.
5
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SRC kinase-mediated parallel activation of prostaglandin and constitutive nitric oxide synthase pathways in leptin protection of gastric mucosa against ethanol cytotoxicity

84%
Slomiany B. L., Slomiany A.
Journal of Physiology and Pharmacology
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2008
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tom 59
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nr 2
Advances in understanding the functional aspects of leptin in the processes affecting peripheral tissues have brought to the forefront the role of this pluripotent cytokine in the processes of gastric mucosal defense and repair. Here, we report that leptin protects the gastric mucosal cells against ethanol cytotoxicity. We show that ethanol cytotoxicity, characterized by a marked drop in the mucosal cells capacity for NO production, arachidonic acid release and prostaglandin generation, was subject to suppression by leptin. The loss in countering capacity of leptin on the ethanol-induced cytotoxicity was attained with cyclooxygenase inhibitor, indomethacin and nitric oxide synthase (cNOS) inhibitor, L-NAME, as well as PP2, an inhibitor of Src kinase. Indomethacin caused the inhibition in PGE2 generation, pretreatment with L-NAME led to the inhibition in NO production, whereas PP2 exerted the inhibitory effect on leptin-induced changes in NO, arachidonic acid and PGE2. The leptin-induced changes in arachidonic acid release and PGE2 generation were blocked by ERK inhibitor, PD98059, but not by PI3K inhibitor, wortmannin. Moreover, the stimulatory effect of leptin on the mucosal cells cNOS activity was inhibited not only by PP2, but also by Akt inhibitor, SH-5. Our findings demonstrate that leptin protection of gastric mucosa against ethanol cytotoxicity involves Src kinase-mediated bifurcated activation of MAPK/ERK and Akt that leads to up-regulation of the respective prostaglandin and nitric oxide synthase pathways.
6
Content available remote

Biological activity of Helicobacter pylori components in mammalian cells: is it independent of proteinase-activated receptors?

67%
Sekiguchi F., Matsumoto Y., Maeda Y., Tsubota-Matsunami M., Nishikawa H., Kawabata A.
Journal of Physiology and Pharmacology
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2012
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tom 63
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nr 6
7
Content available remote

Analysis of the effect of neuropeptides and cannabinoids in gastric mucosal defense initiated centrally in the rat

51%
Shujaa N., Zadori Z. S., Ronai A. Z., Barna I., Mergl Z., Mozes M. M., Gyires K.
Journal of Physiology and Pharmacology. Supplement
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2009
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tom 60
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nr 7
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