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)

The phenomenon of the dual reciprocal regulation of succinate dependent 2H+/Ca2+ exchange was studied in heart and liver mitochondria of experimental animals (allogenic heart transplantation in rat; myocardium infarction in rabbits; pulmonary arteria coarctation in dogs) and in liver bioptates from patients with stomach ulcer. Under pathology two coupled but opposite changes (simultaneous activation and inhibition) in succinate dependent Ca2+ transport occur. The inhibition of Ca2+ transport was detected by its elimination with glutamate, being mostly pronounced after cycle of ADP phosphorylation added to suspension of mitochondria. The treatment of animal with 2-oxoglutarate abolished this inhibition. This was not observed in healthy animals. The described phenomenon can prevent hyperactivation of succinate oxidation under strong pathological (distress) influences.
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PMID:[Dual reciprocal regulation of the succinate oxidation system in heart and liver mitochondria in pathological conditions]. 963 17

Prospects for future development in the field of gastrointestinal pharmacology were briefly discussed on the base of the present progress in our own research on animal models of gastric ulcer and the mechanism of gastric acid secretion. We established a few novel methods to induce extensive ulceration restricted to the gastric antral area in rats by a combination of drug-induced vagal stimulation with necrotizing agents or anti-inflammatory drugs, as well as with ammonia in relation to the etiological role of Helicobacter pilori. In these models, it was found that the gastric antral area become sensitive to mucosal aggression under vagal stimulation and refeeding after starvation and that the mucosal primary afferent nervous system was involved in the integration of gastric mucosal defense mechanisms. Among many experimental gastric ulcer models, the gastric antral ulcer is important for future study because of its unique analogy with human ulcer in its location of incidence and pathology. We also established methods to measure gastric acid secretion in the isolated gastric mucosa or whole stomach of rat or mouse, as well as acid secretion in anesthetized rats. By using these methods, the signal transduction route of vagus nerve stimulation to parietal cells was studied. The importance of mediation of enterochromaffin cells in gastric acid secretion was clearly confirmed. In the studies on receptor mechanisms in the central nervous system regulating gastric acid secretion, critical roles of GABA, barbiturate, glutamate, neurosteroids and opioid receptors were clarified. From these results, several remaining problems were suggested and these must be resolved in future research.
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PMID:[Prospects for future development in the pharmacology of gastric ulcer models and of gastric acid secretion in experimental animals]. 1055 77

Previous studies have shown that excitatory amino acids (EAAs) and their receptors may play important roles in the mammalian enteric system. In this study, we investigated whether EEAs, including L-glutamate (L-Glu) and subtypes N-methyl-D-aspartate (NMDA), kainic acid (KA), and quisqualic acid (QA), reduce cyclic AMP (cAMP) levels and play a role in protecting gastric lesions in cold-restraint stress (CRS) mice. First, we found that dose-dependent administration of four selected EAAs significantly attenuated the increase of cAMP content and exhibited a protective effect on the development of gastric lesions induced by CRS. Second, CRS treatment exhibited a decrease of cGMP content and an increase of cAMP content with marked time-dependent changes, and a high cAMP/cGMP ratio in mice gastric mucosa. Third, pretreatment with 0.25 microg/kg or 0.5 microg/kg dibutyryl cGMP (db-cGMP) exhibited protective effects on CRS-induced gastric lesions, with preventive ratios of 24.61% and 35.32%, respectively. Moreover, db-cGMP at 0.5 microgg/kg significantly attenuated the increase in both cAMP content and the cAMP/cGMP ratio in CRS-treated gastric mucosa. In contrast, db-cAMP exhibited no protective effect, and significantly decreased cGMP content and increased the cAMP/cGMP ratio. These results suggest that EAAs significantly reduce CRS-induced gastric ulcers in mice. The possible mechanism of the antiulcer activity of EAAs may be related to a decrease in the cAMP content in the gastric mucosa of mice. In addition, an increase of the cAMP/cGMP ratio significantly involved in CRS-induced gastric ulcer formation in mice.
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PMID:Protective effect of excitatory amino acids on cold-restraint stress-induced gastric ulcers in mice: role of cyclic nucleotides. 1168 Jun 9

Gardeniae Fructus (GF) and carbonized GF (GFC) have been shown to exert a gastrointestinal protective effect and are frequently used in clinical practice for the treatment of hemorrhage and brown stool. In this study, we employed a combination of pharmacological methods and metabolomics in a rat model of ethanol-induced acute stomach ulcer to investigate the gastroprotective effect of GF and GFC water extracts and the potential mechanism involved in this process. The levels of nitric oxide (NO) and interleukin 6 (IL-6) in the plasma of rats were determined. The results showed that both GF and GFC reduced the ethanol-induced gastric lesions and expression of NO and IL-6 in these rats. Of note, 16 and 11 feature metabolites were filtered and identified in the GF and GFC groups, respectively. Both GF and GFC act by restoring the biosynthesis of valine, leucine, and isoleucine, and the metabolism of glycerophospholipids. Moreover, histological evaluation revealed that heat processing of GF to create GFC enhanced the gastric mucosa protective effect. Furthermore, heat processing converted the main pathway from alanine, aspartate, and glutamate metabolism, associated with GF, to histidine metabolism, associated with GFC. GF and GFC ameliorated gastric mucosa lesions in rats via reductions in NO production and inflammatory cytokine secretion, and the induction of prostaglandin E2.
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PMID:Treatment Mechanism of Gardeniae Fructus and Its Carbonized Product Against Ethanol-Induced Gastric Lesions in Rats. 3133 66