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 role of mucosal mast cells (MMC) in chronic non-allergic reactions of the gastric mucosa is unknown. The present study aimed to investigate the reaction of gastric MMC during healing of the acetic acid-induced gastric ulcer in the rat. Mast cells were stained with toluidine blue and alcian blue+safranin and their density and distribution were assessed. Morphometry of MMC and documentation of their contact with eosinophils were based on electron microscopy. In the normal non-injured rat oxyntic mucosa MMC are grouped in two populations: MMC1 concentrated near the glandular necks, and MMC2 in the basal lamina propria. There was a significant decrease in the number of MMC2 near the ulcer, whereas MMC1 lost their concentration in the neck zone. Also the MMC/connective tissue mast cells ratio was increased in the gastric wall adjacent to the ulcer. Eosinophils were commonly in close contact with MMC. Eosinophil cytoplasm adjacent to MMC was devoid of organelles, which were accumulated in the central cytoplasm. The significant redistribution of mast cell population as well as numerous close contacts between mucosal mast cells and eosinophils, taking place in the neighborhood of the chronic gastric ulcer, seem to be not only of morphological but also of functional significance.
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PMID:The mast cells and an experimental gastric ulcer. Histochemical, ultrastructural and quantitative study in the rat. 871 89

Oxygen free radicals have been implicated in the pathogenesis of gastrointestinal mucosal injury. However, their effect on the quality of experimental gastric ulcer healing has not been investigated previously. Gastric ulcers were produced on the anterior wall of the stomach of rats by submucosal injection of 20% acetic acid. To investigate the role of oxygen radicals, rats with gastric ulcers were treated with scavengers for 6 weeks. Rats received either a daily dose of 20,000 U/kg of recombinant human Cu,Zn-SOD, a 1% solution of DMSO administered orally ad libitum, or 50 mg/kg/day of allopurinol administered orally. The quality of ulcer healing was evaluated by histologic and biochemical parameters: ulcer area, lipid peroxide levels, abnormality of regenerated mucosa, angiogenesis, and fibrosis as assessed by Azan staining, mucin content as assessed by the PAS-positive area, and polymorphonuclear leukocyte (PMN) infiltration. The treatments with SOD, DMSO, or allopurinol did not affect the ulcer area or lipid peroxide levels in the gastric mucosa, and SOD did not affect the histologic abnormality score, PMN infiltration in regenerated mucosa, the collagen fiber proliferation index, or the PAS-positive mucous score. DMSO and allopurinol significantly increased the collagen fiber proliferation index and the PAS-positive mucous score compared with controls. These results indicate that scavenging hydroxyl radicals or inhibiting xanthine oxidase enhances the quality but not the speed of gastric ulcer healing.
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PMID:Effects of oxygen radical scavengers on the quality of gastric ulcer healing in rats. 877 96

This study aimed to investigate the effect of age on natural ulcer healing and delayed ulcer healing induced by nonsteroidal antiinflammatory drugs, using a rat model. Gastric ulcers were induced in young, adult, and aged rats using serosal or mucosal (kissing ulcers) application of acetic acid. Rats were treated with indomethacin 1 mg/kg/day subcutaneously or vehicle for two weeks. Ulcers were assessed by macroscopic and histological measurements of ulcer size. Ulcer induction was affected by age. Aged rats developed significantly smaller ulcers when induced by serosal application of acetic acid and significantly larger ulcers from mucosal application of acetic acid. However, measurements of ulcer size from both models showed no age-related differences in natural ulcer healing. Similarly, indomethacin-induced delayed gastric ulcer healing was not effected by age. We conclude that there are age-related differences in the development of gastric ulcers but there are no age-related differences in natural or delayed ulcer healing in rats.
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PMID:Influence of age on natural and delayed healing of experimentally-induced gastric ulcers in rats. 879 4

Transforming growth factor beta 1 (TGF-beta 1) has been shown to play a central role in wound healing. This peptide has been detected in the stomach, but no information is available at present whether TGF-beta 1 influences the healing of gastric ulcers and whether the mucosal expression of TGF-beta 1 changes in the course of this healing. In this study, gastric ulcers were induced by serosal application of acetic acid and TGF-beta 1 or vehicle saline was injected twice into the subserosa around the ulcer area, once immediately after ulcer induction and two days later. Local application of TGF-beta 1 led to significant acceleration of gastric ulcer healing. Gastric blood flow at the ulcer margin was significantly higher than that in the ulcer crater but no significant difference was found in this flow between studied groups. Immunohistochemistry showed that the expression of TGF-beta 1 reached the peak at day 2 and then declined in the course of healing. We conclude that TGF-beta 1 accelerates ulcer healing possibly by increasing the formation of granulation tissue and cell migration probably mediated by locally expressed TGF-beta 1 but the healing effects of TGF-beta 1 do not depend on the vascular factor.
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PMID:Subserosal application of transforming growth factor-beta 1 in rats with chronic gastric ulcers: effect on gastric ulcer healing and blood flow. 887

The study was performed to examine whether indomethacin administered during the initial period of acetic acid-induced gastric ulcer healing affects future ulcer recurrence. Gastric ulcers were produced in rats by subserosal injection of acetic acid. Indomethacin (1 mg/kg/day, orally) administered either alone or concomitant with ornoprostil (50 micrograms/kg/day, orally) was started on the fourth day and continued for 56 days. In rats whose ulcer healed at the 90th day after production of ulcer, endoscopy was done every 30 days to examine recurrence of ulcer. Gastric specimens were obtained 10, 30, 60, 90, and 240 days after ulcer production for histology, to quantitate the height of regenerated mucosa, thickness of fibrous tissue, degree of polymorphonuclear cell infiltration, and PAS-positive cells. Cumulative ulcer recurrence rate was significantly higher in rats initially treated with indomethacin than in controls. Increased polymorphonuclear cell infiltration was the major histologic abnormality persisting after cessation of indomethacin. Ornoprostil reversed these abnormalities caused by indomethacin. In conclusion, the administration of indomethacin during the initial period of the ulcer healing promoted persistent polymorphonuclear cell infiltration and increased ulcer recurrence rates, possibly via a prostaglandin-dependent mechanism.
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PMID:Indomethacin treatment during initial period of acetic acid-induced rat gastric ulcer healing promotes persistent polymorphonuclear cell-infiltration and increases future ulcer recurrence. Possible mediation of prostaglandins. 888 21

To assess the mechanism of the effect of cigarette smoke on ulcer disease we employed a rat model in which cigarette smoke increases the size of acetic acid-induced gastric ulcer and decreases the hyperemia at the ulcer margin. We postulate that cigarette smoke increases angiotensin II (a vasoconstrictor) in ulcer tissue. Since direct measurement of angiotensin II in small tissue samples is problematic, we compared the messenger ribonucleic acid (mRNA) for its precursors (angiotensinogen and renin) in ulcer and normal gastric tissue. We also evaluated the effect of enalapril, which blocks the conversion of angiotensin I to angiotensin II on ulcer size. In the ulcer tissue, cigarette smoke produced a significant increase in mRNA for angiotensinogen but not for renin. Enalapril decreased the size of the gastric ulcer in rats exposed to cigarette smoke. The data support the possibility that in ulcer tissue cigarette smoke stimulates an angiotensin II-mediated mechanism, which may in part be responsible for the impairment of ulcer margin hyperemia and aggravation of ulcer size.
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PMID:Cigarette smoke increases gastric ulcer size in part by an angiotensin II-mediated mechanism in rats. 900 18

Recently, it has been pointed out that growth factors play an important role in the healing of gastrointestinal ulcers. In the present study, we examined the role of endogenous basic fibroblast growth factor (bFGF) in the healing of gastric ulcers in the rat. In male SD rats, gastric ulcers were induced in the antrum by injection of acetic acid. Time-dependent changes in the area and bFGF content in the ulcerated area and distribution of bFGF in the ulcerated mucosa were examined. Effects of bFGF mutein CS23 (TGP-580) and a monoclonal antibody for bFGF (MAb 3H3) on the healing of the gastric ulcers and angiogenesis in the ulcer bed were also examined. The content of bFGF in the ulcerated area increased with time as the ulcer healed and reached a maximum 7 days after ulcer formation. In the gastric ulcer bed, many cells such as fibroblasts and macrophages were positively stained immunohistochemically by anti-bFGF antiserum. MAb 3H3 (0.1 mg/rat/day, i.v.) inhibited angiogenesis in the ulcer bed and significantly delayed ulcer healing, while TGP-580 (0.001-0.1 mg/kg x 2/day, p.o.) increased the number of microvessels in the ulcer bed and accelerated the healing. These results suggest that endogenous bFGF may play an important role in the healing of gastric ulcers in the rat and that the angiogenic properties of bFGF (TGP-580) may be involved in its effect on ulcer healing.
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PMID:Role of endogenous basic fibroblast growth factor in the healing of gastric ulcers in rats. 903 35

The action of Codonopsis pilosula extract in 5 animal models of gastric ulcer was investigated. It was found that the extract had higher efficacy on gastric ulcer induced by stress, acetic acid and sodium hydroxide and little significant effect on ulcers induced by pyloroligature and indomethacin. The C. pilosula extract was also capable of reducing gastric acid pepsin secretion. It is possible that inhibition of gastrointestinal movement and propulsion is one of the mechanisms underlying the antiulcer action of C. pilosula extract.
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PMID:Investigations on the protective action of Condonopsis pilosula (Dangshen) extract on experimentally-induced gastric ulcer in rats. 906 93

This study was done to investigate the gene expression and localization of tenascin in ulcerated gastric tissues during the healing process with Northern blot analysis and immunohistochemical technique. Gastric ulcers in rats were produced by acetic acid. Tenascin mRNA levels in the ulcerated tissue were significantly increased in a biphasic manner (12 h and day 5), preceding the increase in collagen type IV and laminin mRNA levels, and returned to control levels on day 11. In intact tissues, tenascin was mainly localized in the basement membrane above the proliferative zone, in contrast to the predominant localization of collagen type IV and laminin below the proliferative zone. On the ulcer margin from 12 h to day 5, tenascin was abundantly observed in the lamina propria around nonproliferating new epithelial cells, but collagen type IV and laminin were not seen in this lamina propria. On day 7, tenascin, expressed in the lamina propria, was replaced by collagen type IV and laminin. Thus, the rapid expression and unique localization of tenascin suggest the important role of tenascin in gastric ulcer healing.
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PMID:Rapid expression and specific localization of tenascin in gastric ulcer healing in rats. 914 1

The hepatocyte growth factor has been reported to be a potent mitogen of various epithelial cells, including gastric mucosal cells. Therefore, production and activation of hepatocyte growth factor in the gastric wall were investigated to speculate on the possible role of this factor in the healing of gastric ulcer in rats. Indomethacin-induced gastric mucosal lesions and acetic acid induced ulcers were employed as models of acute gastric lesions and chronic ulcer, respectively. Immunoblot and Northern blot analyses indicate that experimentally induced gastric mucosal lesions stimulate not only the production of hepatocyte growth factor, but also the conversion to its active form. This conversion was accompanied by increased gene expression of hepatocyte growth factor activator in the stomach. In rats with acute mucosal lesions, hepatocyte growth factor activator mRNA was most abundant 6 h after induction of mucosal lesions. On the other hand, hepatocyte growth factor and hepatocyte growth factor activator mRNA levels were elevated until 15 days after the induction of chronic ulcers. In summary, it has been clarified that not only production, but also activation of hepatocyte growth factor is stimulated during gastric ulcer healing.
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PMID:Production and activation of hepatocyte growth factor during the healing of rat gastric ulcers. 924 17


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