Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sodium polyacrylate (PANa) is a water-soluble, high-molecular compound, and its aqueous solution shows a very high viscosity and stringiness. In the present study, preventive effects of PANa on three kinds of esophageal lesions induced by gastric juice were examined in comparison with those of aceglutamide aluminum and sodium alginate. The influences of PANa on gastric contents were also studied. The preventive effect of PANa given intraesophageally on esophageal lesions induced by the intraesophageal application of gastric juice was more potent than aceglutamide aluminum and sodium alginate. Oral administration of PANa inhibited the formation of esophageal ulcer by pylorus ligation more markedly than aceglutamide aluminum, whereas sodium alginate had no effect in a high dose of 500 mg/kg. In preventing gastric ulcer which occurred simultaneously with the esophageal ulcer after the pylorus ligation, aceglutamide aluminum was most potent, and PANa was as potent as sodium alginate. Oral administration of PANa showed a more protective effect than aceglutamide aluminum on the esophageal ulceration induced by the simultaneous ligations of the pylorus and limiting ridge, whereas sodium alginate in a high dose of 500 mg/kg had little effect on the ulcer formation. PANa caused only a slight increase in the pH of gastric juice and a slight decrease in pepsin activity. From the results, it may be concluded that PANa showed an antiulcerogenic activity mainly due to its mucosa covering action against gastric juice.
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PMID:Effects of sodium polyacrylate (PANa) on acute esophagitis by gastric juice in rats. 710 49

Recent studies demonstrated that experimental ulcers are associated with changes in the properties of voltage-sensitive sodium currents in sensory neurons. We hypothesized that nerve growth factor (NGF) contributes to these changes. Gastric ulcers were induced by acetic acid injection into the wall of the rat stomach. NGF expression was determined by ELISA and immunohistochemically. Sensory neurons were labeled by injection of a retrograde tracer into the gastric wall. Sodium currents were recorded in gastric sensory neurons from nodose and dorsal root ganglia cultured for 24 h in the presence of NGF or a neutralizing NGF antibody, respectively. Gastric ulcer formation caused a rise in NGF concentration within the gastric wall and an increase in NGF immunoreactivity. Exposure to NGF caused a significant increase in the TTX-resistant sodium current, whereas the TTX-sensitive sodium current remained unchanged. This was associated with an acceleration of the recovery from inactivation in spinal sensory neurons. Production and release of NGF in the gastric wall may contribute to sensitization of primary afferent neurons during gastric inflammation.
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PMID:Role of nerve growth factor in modulation of gastric afferent neurons in the rat. 1257 6