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)

Effects of treatment with free radical scavengers in the healing process of acetic acid-induced gastric ulcer on the ulcer aggravation induced by indomethacin were investigated. Gastric ulcers were produced on the anterior wall of the stomach of male Sprague-Dawley rats by submucosal injection of 20% acetic acid. To investigate the role of oxygen radicals, rats with gastric ulcer were treated with scavengers for six weeks and then treated with indomethacin (1 mg/kg/day). While superoxide dismutase (10,000 units/kg/day) did not affect the ulcer area after indomethacin treatment, allopurinol (50 mg/kg/day) slightly inhibited the increase in ulcer area. Dimethyl sulfoxide (1% solution, ad libitum) produced a significant decrease in size of the ulcer after indomethacin treatment. Increased lipid peroxides in the gastric mucosa after indomethacin treatment decreased significantly in the rats of the dimethyl sulfoxide and allopurinol groups. These results indicate that lipid peroxidation mediated by oxygen radicals plays an important role in the mechanism of ulcer aggravation induced by indomethacin.
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PMID:Effects of free radical scavengers on indomethacin-induced aggravation of gastric ulcer in rats. 755 59

This study was done to elucidate whether rebamipide during the initial period of acetic acid-induced gastric ulcer affected healing and future ulcer relapse. The cumulative healing rate was higher in rats given rebamipide alone or those given rebamipide and cimetidine during and after administration, but not in rats given cimetidine alone, compared to control rats. Cumulative relapse rate was significantly lower in rats initially given rebamipide alone or those given rebamipide and cimetidine than in rats initially given cimetidine alone. These results suggest that rebamipide is beneficial for obtaining a better quality of ulcer healing and reduction of future ulcer relapse.
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PMID:Rebamipide, novel prostaglandin-inducer accelerates healing and reduces relapse of acetic acid-induced rat gastric ulcer. Comparison with cimetidine. 758 34

Basic fibroblast growth factor (bFGF) has well-established angiogenic and ulcer healing actions. bFGF has also been found to induce neural regeneration in the central nervous system. Thus, the present study was undertaken to clarify the effect of basic fibroblast growth factor on the regeneration of autonomic nerves in the granulation tissues following the induction of experimental gastric ulcer induced by acetic acid in rats. Rats were divided into control, acetic acid alone, and acetic acid plus acid-stable human recombinant basic fibroblast growth factor (CS23, 1 microgram/100 g body wt., every 12 hr for three days, or one or two weeks, through oral gastric intubation) groups. As a result, few autonomic nerves were recognized surrounding the newly formed arterioles and venules in the acetic acid alone group. In the CS23-treated group, the cholinergic, calcitonin gene-related peptide and vasoactive intestinal peptide-immunoreactive nerves were clearly recognized near the microvessels, but few adrenergic nerves were seen even after CS23 treatment. From these observations, basic fibroblast growth factor was suggested to promote the reinnervation of the newly formed microvessels.
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PMID:Effect of basic fibroblast growth factor on reinnervation of gastric microvessels. Possible relevance to ulcer recurrence. 762 67

The healing of acetic acid-induced gastric ulcer in rats and the effects of cimetidine and calcitonin were investigated with reference to the enzyme activity of both prolylhydroxylase and collagenase as related to histological findings. The rats were observed by endoscopy on the 3rd day after the subserosal injection of acetic acid; rats with ulcers were divided into three groups: non-treated, and cimetidine- and calcitonin-treated. The latter two groups were treated for 7 days. Prolylhydroxylase activity in active ulcers in the non-treated group was slightly higher on the 3rd day and significantly higher on the 10th day than the activity in control rats that had received subserosal injections of physiological saline solution on the respective days. In non-treated rats, the healed ulcer on the 10th day showed lower prolylhydroxylase activity than that in the active ulcer on the same day. Cimetidine did not affect prolylhydroxylase activity, but, with calcitonin, there was higher prolylhydroxylase activity in the healed than in the active ulcer, although the difference was not significant. Interstitial collagenase showed the highest activity on the 3rd day and decreased on the 10th day in non-treated rats. Collagenase activity was higher in the cimetidine-treated group, than that in the non-treated group, and numerous peroxidase-positive granulocytes were seen in the mucosa and submucosa. Calcitonin did not affect collagenase activity. The participation of both enzymes is indispensable in the healing process and the effects of anti-ulcer agents on these enzymes must be considered.
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PMID:Wound healing of acetic acid-induced gastric ulcer in rats and the effects of cimetidine and calcitonin, with special reference to prolylhydroxylase and collagenase enzyme activity. 764 95

We determined the kinetics and phenotypes of infiltrating B cells in gastric ulcer in the rat induced by gastric injection of acetic acid (day 0). Few B cells were found in the lesion in the early stages of ulceration. On day 40, two kinds of B cells with phenotypes of IgMhighIgDlowOX33 (CD45)+OX19 (CD5)- and IgMlowIgDhighOX33 (CD45)+OX19 (CD5)- were scattered in the granulation tissue of open ulcers, but not in the healed scar tissue. On day 180, those two kinds of B cells formed primary follicles in the granulation tissue of open ulcers, but were absent from the healed scar tissue. The IgMhighIgDlowOX33 (CD45)+OX19 (CD5)- B cell was considered to be identical to the marginal zone B cell of rat spleen. This phenotype of B cell might be associated with inflammatory process in chronic gastric ulcer.
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PMID:Two phenotypically distinct B lymphocytes (IgMhighIgDlow and IgMlowIgDhigh) in chronic gastric ulcer in the rat. 769 15

In this study we characterized the effects of a novel anti-inflammatory drug, ML 3000 ([2,2-dimethyl-6-(4-chlorophenyl)-7-phenyl-2,3-dihydro-1H-pyrrolizine- 5-yl]-acetic acid), on the gastric mucosa and attempted to determine the mechanism responsible for its apparent stomach-sparing properties. Acute gastric damaging properties of ML 3000 versus indomethacin were examined in the rat, while chronic-type gastric ulcer was examined in the rabbit. At doses of up to 100 mg/kg p.o., ML 3000 did not produce significant acute gastric injury, while indomethacin at 5-20 mg/kg p.o. caused mucosal necrosis and bleeding. ML 3000 significantly inhibited gastric and blood prostaglandin E2 synthesis, with the higher doses tested (30 and 100 mg/kg) producing comparable effects to that seen with indomethacin at 10 or 20 mg/kg. Gastric and blood leukotriene B4 synthesis were not significantly affected by either drug. While indomethacin caused a significant increase in leukocyte adherence to mesenteric venules, ML 3000 did not. When administered repeatedly to rabbits, diclofenac caused penetrating ulcer formation in the gastric antrum of the majority of the animals. ML 3000 did not produce any detectable damage at doses of 10 or 30 mg/kg, but an ulcer was observed in one of five rabbits given the 100 mg/kg dose. Prior administration of ML 3000 (10-100 mg/kg) did not significantly affect the extent of gastric damage induced by subsequent oral administration of ethanol. These studies demonstrate that ML 3000 spares the gastric mucosa despite significantly suppressing gastric prostaglandin synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:ML 3000 reduces gastric prostaglandin synthesis without causing mucosal injury. 770 53

The effects of IGN-2098 on the healing process of acetic acid-induced gastric ulcer was investigated in comparison with the other histamine H2-receptor antagonists, famotidine and roxatidine acetate HCl, in rats. Ulcer was induced by the injection of acetic acid solution (20%, 0.05 ml). From the 4th day to 17th day after the ulcer induction, drugs were orally administered twice a day. On the 18th day after the ulcer induction, rats were sacrificed to measure the ulcer index macroscopically and to take pictures of the stomachs. Judging from the photographs, the prominence of ulcer the edge was graded into 4 classes, which showed a significant correlation with the histological amount of connective tissue at the ulcer edge. All drugs accelerated the healing of the ulcer, and the effect of IGN-2098 was the most remarkable. In addition, IGN-2098-treatment exhibited more marked inhibition against the prominence of the ulcer edge as compared with the control group. Based on these results, it is concluded that IGN-2098 may be a useful drug for the clinical treatment of ulcer and that the healing acceleration by IGN-2098 without prominence of the ulcer edge may induce no relapse of the ulcer after healing.
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PMID:[Therapeutic effect of IGN-2098, a new antiulcer drug (H2-antagonist), in the ulcer diminishing period against acetic acid-induced gastric ulcer in rats]. 772 Nov 93

We examined the effect of a liquid diet or a combined diet of liquid plus cellulose on the healing of gastric ulcers induced in rats in comparison with that of solid chow. Ulcers were induced in the fundus of the stomach by luminal application of an acetic acid solution. The healing of ulcers could be divided into two phases based on the healing rate: early phase (days 1 to 10) and late phase (days 10 to 20). The liquid diet, but not the combined one, administered for 10 days significantly accelerated ulcer healing in both the early and late phases. The length of the ruptured muscularis mucosa decreased only in the liquid diet group in both phases. Regeneration of the ulcerated mucosa in the chow diet group was observed only in the late phase, it being markedly inhibited in the liquid diet group. The serum gastrin level significantly decreased in the liquid and combined diet groups in contrast to that in the chow group. The liquid and combined diets significantly reduced gastric mucosal DNA synthesis. We conclude that 1) the healing in this gastric ulcer model comprises two phases, and 2) tissue contraction is a major factor for the healing of gastric ulcers in the early phase, while both tissue contraction and regeneration of the ulcerated mucosa are involved in the healing in the late phase.
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PMID:Acceleration of healing of gastric ulcers induced in rats by liquid diet: importance of tissue contraction. 772 15

Zinc is an important element in wound healing. Zinc compounds hasten the healing of gastric ulcers, by an unknown mechanism(s). We studied the effect of the induction of zinc deficiency on gastric ulcer healing. Rats were given a control or zinc-deficient diet for six weeks and then subjected to the induction of acetic acid-induced chronic gastric ulcers. Four days later, zinc-deficient rats were divided into two groups. In the first group, the zinc-deficient diet was continued. In the second group, the diet was changed to the control diet. Zinc-deficient rats had a mean serum zinc concentration approximately 70% of that in controls. Zinc deficiency did not affect the formation of gastric ulcers; however, it reduced cell proliferation by day 4 and delayed ulcer healing. Zinc supplementation brought zinc to control levels within a week, but failed to reverse the delay in ulcer healing. We conclude that zinc is crucial for healing of gastric ulcers, especially at the early stage.
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PMID:Zinc deficiency delays gastric ulcer healing in rats. 778 57

The anti-ulcer effects of bifidobacteria, lactobacilli and streptococci were examined using the acetic acid-induced gastric ulcer and ethanol-induced erosion models in rats. Bifidobacterium breve YIT4014 and 4043, and Bifidobacterium bifidum YIT4007 were administered orally, and anti-ulcer effects were confirmed for not only these organisms but also their polysaccharide fractions (PSFs). The major component of these anti-ulcer polysaccharides was rhamnose. In particular, polysaccharides in which the rhamnose content exceeded 60% were more effective in healing gastric ulcers. After administration of the PSF from B. bifidum YIT4007, the levels of epidermal growth factor and basic fibroblast growth factor increased in gastric tissues. Similar results were observed for the culture supernatant of gastric epithelial cells cultured with PSF. Furthermore, the production of 6-ketoprostaglandin F1 alpha by macrophages was also enhanced by PSF. These results indicated that these bacteria and their polysaccharides induced host repair and protective systems in the gastric ulcer model.
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PMID:Anti-ulcer effects of lactic acid bacteria and their cell wall polysaccharides. 782 99


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