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)

Anti-ulcerogenic effects of trimoprostil, a prostaglandin E2 (PGE2) derivative, were studied in comparison with those of PGE2, cimetidine and sulpiride. Trimoprostil and PGE2 given p.o. prevented the formation of gastric lesions produced by absolute ethanol, 0.2N NaOH, 0.6N HCI and hypertonic NaCl solutions in rats and aspirin-induced fecal occult bleeding in dogs. Although both prostaglandins did not alter the gastric mucus content, they equivalently prevented the stress-induced decrease in the mucus content in rats. The duration of these effects of trimoprostil was longer than those of PGE2. Cimetidine and sulpiride did not exert such cytoprotective effects. Trimoprostil inhibited stress-induced gastric ulcer formation in rats more markedly than PGE2, cimetidine and sulpiride. Trimoprostil and PGE2 at the cytoprotective dose (30 micrograms/kg, p.o.) did not change the gastric blood flow in conscious rats. In Shay rats, trimoprostil at doses larger than the cytoprotective doses inhibited the gastric acid secretion when given p.o., but was not effective when given i.d. PGE2 exerted the similar action, but the potency was clearly weaker than that of trimoprostil. In Heidenhain-pouch dogs, trimoprostil also inhibited the gastric acid secretion stimulated by pentagastrin more markedly than did cimetidine. In conclusion, trimoprostil at doses smaller than the antisecretory doses exerted gastric cytoprotective action with a longer duration than that of PGE2, probably through the preservation of the mucus barrier. Such cytoprotection was not found with cimetidine and sulpiride.
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PMID:[Anti-ulcerogenic and cytoprotective effects of trimoprostil (Ro 21-6937), a trimethylprostaglandin E2 derivative]. 660 97

The secretion of gastric juice, HCI, and sialic acid was investigated in 45 patients with chronic renal failure, 13 patients with gastric ulcers, 52 with duodenal ulcers, and 27 control patients during the dose-response pentagastrin test. The renal patients had low gastric juice and HCI secretion both in the basal condition and during pentagastrin stimulation. It was almost of the same magnitude as in patients with gastric ulcers. The basal sialic acid secretion in renal patients did not differ from that of the controls, but in patients with peptic ulcers it was significantly higher. During pentagastrin stimulation the differences decreased. Stimulated maximal HCI output values in relation to sialic acid output were also similar in the gastric ulcer and renal patients. Thus the gastric secretion profiles, excluding the basal sialic acid secretion, were quite alike in patients with chronic renal failure and those with gastric ulcers.
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PMID:The gastric secretion profile of patients with chronic renal failure. 723 12

The quality of ulcer repair remains crucial for the stability of the injured tissue and for preventing recurrence. Therefore, we studied the temporo-spatial expression of the fibrillar and basement membrane collagens (types I, III, and IV), the collagenase MMP-2 as well as its inhibitor TIMP-1 before and after oral administration of basic fibroblast growth factor (b-FGF) over 30 days in acetic acid-induced rat gastric ulcers. The alterations and the exact location of the mRNA transcripts and their precipitated proteins were visualized by means of radioactive in situ hybridization and immunohistochemistry. Our data show that hybridization signals of procollagen I could first be identified 2 hours after ulcer induction. After 12 hours the ulcer was established and the mRNA was enhanced at the ulcer margin. After 24-48 hours the other procollagen transcripts were detected and all were further upregulated over the mesenchymal cells of all gastric layers up to 21 days, then declined at 30 days. In contrast, MMP-2 became prominent after 48 hours and up to 21 days. TIMP-1 was enhanced at 72 hours. After oral administration of b-FGF the transcriptional activity of the procollagens and MMP-2 was not significantly altered, while ulcer diameter was significantly reduced. We conclude that the early onset and long duration of collagens' expression points to their central structural and functional role in gastric ulcer healing. MMP-2 seems to be involved in both active ulceration and ECM remodeling. The timing of TIMP/MMP expression may be critical for proper restoration of gastric wall integrity.
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PMID:Remodeling of extracellular matrix in gastric ulceration. 1152 57

In the assessment of the functional state of the stomach the interest to its secretory functioning has remained constant and in the center of attention of physiologists and clinicians during the past century. That is understandable. After all, the level of secretion of gastric juice enriched with the acid and pepsins defines numerous aspects in the functioning of this organ and its peptic, bactericidal and even evacuation functions. Moreover, under certain conditions active gastric juice can turn from a mediator in the normal peptic process into a solely pathogenetic factor and promote the development of a number of so-called acid-dependent diseases that have conventionally included stomach ulcer, reflux-esophagitis, postgastrectomy ulcers of the anastomosis and other more infrequent pathological states. A distinct positive reaction to the application of anti-acid preparations is common for all these diseases. At the same time, the role of HCI in their development remains comprehensible only in some aspects.
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PMID:[Problems of functional study of the stomach in contemporary gastrology]. 1261 69

The gastroprotective activity of phytosphingosine hydrochloride (PS-HCl, CAS 554-62-1) was assessed in four different rat models of experimentally induced gastric ulcer. Various doses (2.5-10 mg/kg) of PS-HCI were orally administered to rats 30 min before the treatment with HCl/ethanol, indometacin, cysteamine, or to rats with ligated pylorus. Oral administration of PS-HCl (2.5-10 mg/kg) to rats prevented the acute ulcer formation in 4 different types of ulcer in a dose-dependent manner as follows: (1) HCl/ethanol-induced gastric mucosal membrane lesions (20.1-47.8% inhibition), (2) indometacin-induced gastric mucosal membrane lesions (4.6-31.9% inhibition), (3) duodenal ulcer induced by cysteamine (10-20% inhibition), (4) gastric secretion and ulceration following pylorus ligation (33.3-61.9% inhibition). These results indicate that PS-HCI may be useful for the prevention of gastric ulcer.
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PMID:Anti-ulcer actions of phytosphingosine hydrochloride in different experimental rat ulcer models. 1614 14

Matrix metalloproteinases (MMPs) play an important role in degradation of gastric extracellular matrix proteins. However, no reports are available on the relationship between the activity of MMPs and gastric ulceration induced by alcohol. Our objective was to investigate the effect of melatonin (N-acetyl-5-methoxytryptamine) on the regulation of MMP-9 and MMP-2 activities during prevention of ethanol-induced gastric ulcer. Biochemical and zymographic methods were used to analyze MMP-9 and -2 activities in gastric tissues of Balb/c mice following induction of gastric ulcer by ethanol. Our studies reveal that melatonin arrested cell injury, protein carbonyl formation, and lipid peroxidation in mice during gastroprotection. Melatonin dose-dependently reduced proMMP-9 activity that was induced ( approximately 25-fold) during ethanol-induced gastric ulceration. Severity of gastric ulcers were correlated proportionately with increased dose of ethanol and elevated activity of proMMP-9 and -2. The reduced activities of MMP-9 and -2 were associated with reduced expression of TNF-alpha and increased expression of tissue inhibitors of metalloproteinases (TIMP-1 and TIMP-2). We conclude that melatonin's ability to prevent ethanol-induced gastric ulceration in mice is related to a reduction in proMMP-9 activity and expression.
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PMID:Matrix metalloproteinase-9 activity and expression is reduced by melatonin during prevention of ethanol-induced gastric ulcer in mice. 1761 36