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 aims of our experiments were to clear up the possible correlations between the free radical mechanisms and the gastric cytoprotection of beta-carotene on HCl-induced gastric mucosal lesions. The beta-carotene was intragastrically given in doses of 1 and 10 mg/kg and 30 min. later 1 ml 0.6 N HCl was given to provoke the mucosal damage. After 1, 5, 15, 30 and 60 min. the animals were sacrificed. The number and severity of gastric mucosal lesions were calculated. The superoxide dismutase (SOD), glutathion peroxidase (GPX), catalase (CAT) activity and the malondialdehyde (MDA) and reduced glutathion (GSH) contents were determined from the gastric mucosa of rats. It was found that 1. beta-carotene was able to reduce the number and severity of ulcers only after 30 min.; 2. the CAT activity was decreased at 60 min. by carotene; 3. the GPX activity became dissimilar in the different groups after 15 min; 4. the changes of GSH were found to be similar ones; 5. the SOD activity was lower during the cyto-protection; 6. the MDA level remained practically unchanged. It has been concluded that 1. the free radicals are the consequences of the development of gastric ulcer and cytoprotection; 2. the scavenger character of beta-carotene is involved in its cytoprotective effect.
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PMID:The free radical mechanisms in beta-carotene induced gastric cytoprotection in HCl model. 259 22

Glycyrrhetinic acid (Ia) and eighteen related derivatives were examined for antiulcer activity using stress-induced gastric lesions (restraint plus water immersion at 25 degrees C) in mice and rats as screening tests. Among the compounds tested, dihemiphthalate derivatives of 18 alpha- or 18 beta-olean-12-ene-3 beta,30-diol (IV, IIId), 18 beta-olean-9(11)12-diene-3 beta,30-diol (VIc), and olean-11,13(18)-diene-3 beta,30-diol (VIIc) showed potent inhibition of gastric lesion formation at a dose of 12 or 25 mg/kg (p.o.); carbenoxolone sodium (Ib) significantly suppressed the lesion formation at a dose of 500 mg/kg (p.o.). Further evaluation of the antiulcer activity was carried out mainly for compound IIId. Compound IIId (p.o.) prevented the formation of indomethacin-induced or 0.6 N HCl-induced gastric lesions; the latter antiulcer effect was noted even in the combined treatment with indomethacin, suggesting that the effect occurs independently of endogenous prostaglandins. In contrast, compound IIId had no preventive effect against Shay rat ulcer when intragastrically (i.g.) administered; further, no antisecretory effect was seen by i.g. application in pylorus-ligated rats. Administration of compound IIId for 2 weeks accelerated the healing rate of acetic acid-induced gastric ulcer in rats. No significant change in urine excretion was observed after its consecutive administration for 3 d. These results suggest that dihemiphthalate derivatives (IIId, IV, VIc, VIIc) may produce a strong antiulcer activity, probably by strengthening some gastric mucosal defensive mechanism.
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PMID:Antiulcer activities of glycyrrhetinic acid derivatives in experimental gastric lesion models. 260

The aetiology of ethanol-induced gastric ulceration, and its interaction with zinc, were studied in rats. Oral administration of ethanol (40, 50 or 80%) to conscious rats reduced the stomach mucus content and increased gastric ulcer formation in a concentration-dependent manner. Histological examination indicated that mucus, both on the surface and within the epithelium, was depleted because of epithelium being shed from the gastric mucosa. Zinc sulphate abolished mucus loss and ulcer formation in the ethanol-treated animals. Using an ex-vivo gastric chamber preparation in anaesthetised animals, it was found that an ethanol (50%)-HCl (100 mmol/l) solution produced severe glandular haemorrhagic ulceration, elevated Na+, K+ and protein levels in the luminal solution, and reduced the H+ content in this fluid. Zinc sulphate pretreatment dose-dependently prevented all these changes. On the other hand, prostaglandin E2 (PGE2) administration only antagonised ethanol ulceration and H+ loss from the chamber; it did not significantly influence the Na+ and K+ fluxes and protein leakage into the luminal solution. It is concluded that the antiulcer mechanisms of zinc sulphate and PGE2 may be different. Protection by the former drug could be due partly to preservation of mucus adhering to the gastric mucosa. The possibility of the membrane-stabilising action of zinc contributing to the observed effects is also discussed.
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PMID:Protection by zinc sulphate against ethanol-induced ulceration: preservation of the gastric mucosal barrier. 294 51

A randomized, double-blind, placebo-controlled trial was conducted to determine the efficacy of a low-dose aluminum-magnesium antacid regimen (Link one tablet q.i.d.) (total neutralizing capacity 120 mmol HCl/day) in combination with a high- or a low-fiber diet in ulcer healing and relief of symptoms in patients with benign gastric ulcer. After 6 wk, the ulcer healed in 28 (67%) of the 42 patients treated with antacids compared with 11 (25%) of the 44 patients treated with placebo (p less than 0.001). Antacids were also significantly more effective than placebo in the relief of symptoms. The dietary treatment did not significantly influence ulcer healing or ulcer symptoms. Constipation was more frequently seen with the low- than with the high-fiber diet (p less than 0.01). No significant side effects from antacids were recorded.
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PMID:Healing of benign gastric ulcer with low-dose antacids and fiber diet. 301 83

A metallothionein isoform metallothionein-II was isolated from the livers of zinc acetate-treated rats. Metallothionein-II, which showed a single band on polyacrylamide gel electrophoresis, was subjected to two kinds of anti-ulcer screening systems. It was shown that intravenously administered metallothionein-II suppressed the formation of rat water-immersion stress- and HCl-ethanol-induced gastric ulcer significantly. The effect may partly be derived from the zinc contained in the metallothionein-II. However, the effect of metallothionein-II was much stronger than that of an equivalent mole of zinc. Apparently, metallothionein-II had an anti-ulcerogenic activity not based on the effect of intrinsic zinc.
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PMID:Suppression of gastric ulcer induced by stress and HCL-ethanol by intravenously administered metallothionein-II. 334 6

The glyceroglucolipids content of basal and pentagastrin-stimulated gastric secretion was measured in male patients with gastric (12) and duodenal (12) ulcer. Six patients in each group received twice daily for a period of 4 weeks 150 mg of ranitidine, whereas the other patients received placebo. The glyceroglucolipids output in the basal secretion of patients with gastric and duodenal ulcer before treatment was similar and increased 2.7-fold after pentagastrin stimulation. In all patients treated with ranitidine, the mean output of glyceroglucolipids after pentagastrin stimulation increased from 1.38 to 2.05 mumol/h (P less than 0.05). This increase, however, was more pronounced in the duodenal ulcer group than in the gastric ulcer patients. No change in glyceroglucolipids output was noted in the patients treated with placebo. The ratio of glyceroglucolipids to HCl increased significantly (P less than 0.02) only in the ranitidine-treated patients.
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PMID:Effect of ranitidine on the content of glyceroglucolipids in gastric secretion of patients with gastric and duodenal ulcer. 608 4

Cysteamine given three times within 8 h produced severe duodenal and gastric ulcers in female SIV rats. A pentobarbital anesthesia during the first 10 h prevented gastric ulcer formation without affecting duodenal ulcer. An additional 10 h lasting intragastric infusion with 0.6 ml/h Ringer containing 5 mmol/l of a mixture 3: 1 pure taurocholic and glycocholic acid or 20 and 50 mmol/l pure taurocholic acid in 0.2 N HCl did not reverse the protective effect of pentobarbital, e.g. incidence and intensity of gastric ulcer did not change. Treatment with somatostatin significantly reduced the intensity of duodenal ulcer. The inhibition of cysteamine-induced gastric ulcer formation by pentobarbital does not seem to be due to a possible inhibition of duodenogastric reflux but more likely to an inhibition of central nervous stress reactions by anesthesia.
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PMID:Effect of pentobarbital anesthesia and bile acids on cysteamine-induced duodenal and gastric ulcers in rats. 614 97

Today, we have effective and potent drugs such as H2-receptor antagonists for the treatment of peptic ulcers. Cimetidine and ranitidine are antisecretory drugs which heal 67-90% of duodenal ulcers in 4 weeks. Certain prostaglandins (PGs) which also heal gastroduodenal ulcers and hemorrhagic gastritis not only diminish gastric acid secretion but also confer unique protective properties on the gastroduodenal mucosa. This phenomenon of 'cytoprotection' is supported by the experimental finding that PGs prevent gastroduodenal mucosal injury caused by absolute ethanol, HCl, NaOH and other irritating agents. Other PGs which do not reduce gastric acid secretion also heal human gastroduodenal ulcers. These special properties of PGs make them potentially beneficial for the treatment of gastric ulcer, and gastroduodenal ulcers accompanying use of nonsteroidal anti-inflammatory drugs as well as hemorrhagic gastritis which is particularly refractory to other therapeutic modalities.
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PMID:Prostaglandins, gastroduodenal ulcer and hemorrhagic gastritis. 633 8

The present study demonstrated that acetazolamide (100 and 200 mg/kg, s.c.) induced severe gastric hemorrhagic ulceration in rats. The ulceration was aggravated by oral administration of HCl, but was inhibited by NaHCO3. Furthermore, the severity of ulceration was also decreased by pretreatment with methysergide, chlorpheniramine, or cimetidine. These protective effects were accompanied by an increase in serotonin and histamine released from the stomach. Acetazolamide injection also increased the protein level but reduced the sialic acid content in the gastric secretion, indicating that the gastric mucosal barrier may have been damaged. Prostaglandin E2 content of the gastric mucosa was not affected by the drug; however, carbonic anhydrase activity was markedly reduced in a dose-dependent manner. Thus, it is suggested that the ulceration induced by acetazolamide is mainly due to the inhibition of carbonic anhydrase activity and mucus secretion. The increase in serotonin and histamine release also may have been the contributing factors for gastric ulcer formation.
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PMID:Study of the damaging effects of acetazolamide on gastric mucosa in rats. 644 31

The effects of three typical antisecretory agents: cimetidine, atropine and prostaglandin E2 were compared on an acute rat gastric ulcer model which consisted of perfusing the stomach continuously, at a high intraluminal pressure (120 mm H2O), with a simulated gastric juice (0.1 M HCl plus 600 mg pepsin/l). As the acid and pepsin are given exogenously the inhibitory action of the antisecretory drugs is obviated in this model. Cimetidine and atropine failed to reduce gastric erosions, whereas prostaglandin E2 markedly reduced the severity of the mucosal lesions with respect to control values. Long-term treatment with cimetidine also failed to increase the resistance of the gastric mucosa to the digestive action of the artificial gastric juice. These findings indicate that only prostaglandin E2 is cytoprotective and do not support the view that anticholinergics or histamine H2-receptor antagonists have a cytoprotective role on the cells of the gastric mucosa.
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PMID:Effects of cimetidine, atropine and prostaglandin E2 on rat mucosal erosions produced by intragastric distension. 744 34


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