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)

To investigate the destructive process of connective tissues in gastric ulcer, both collagenolytic and gelatinolytic activities were examined in the homogenates of rat acetic acid-induced gastric ulcer, a typical model of chronic ulcer. Gelatinolytic activity in the ulcerous lesion was significantly higher than that in the normal tissue. However, collagenase was not detected in both normal and ulcerated tissues either by the enzyme assay or by the immunoblotting. By gelatin-gel-zymographic analyses, the gelatinolytic activity was found to be composed of a number of species, mainly 60-, 72- and 92-kDa, all of which were inhibited by ethylenediaminetetraacetic acid. Among the induced matrix metalloproteinases, one crossreacted with a sheep anti-(rabbit prostromelysin)antibody. Thus, in chronic gastric ulcer, it is likely that several metalloproteinases participate in degradation of connective tissue matrices including components of basement membranes. The elevated levels of gelatinolytic activities in the ulcerous tissues and ulcer index were significantly suppressed by treating the animals with famotidine or a new H2-receptor antagonist, 3-amino-4-[4-[4-(1-piperidinomethyl)-2-pyridyloxy]-cis-2- butenylamino]-3-cyclobutene-1,2-dione hydrochloride (IT-066).
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PMID:Effects of H2-receptor antagonists on matrix metalloproteinases in rat gastric tissues with acetic acid-induced ulcer. 168 58

Single biopsies of human gastric mucosa from controls and different groups of patients were used for enzymatic cell isolation by pronase and collagenase and subsequent count of parietal and nonparietal cells. This procedure was tested in regard to its validity and delivered the following cell numbers. Total gastric cells/mg wet weight gastric mucosa: normal gastric mucosa [controls (C), n = 95] 31,500 +/- (SEM) 1,490, chronic superficial gastritis (GI; n = 49) 36,300 +/- 2,770, chronic gastritis with beginning atrophy (GII; n = 36) 44,100 +/- 3,050 (p less than 0.025), chronic atrophic gastritis (GIII; n = 12) 40,100 +/- 5,760, duodenal ulcer (DU; n = 26) 29,340 +/- 2,280, gastric ulcer (GU; n = 23) 37,090 +/- 3,000, gastric resection according to Billroth I (BI; n = 7) 57,480 +/- 12,360 (p less than 0.005) and Billroth II (BII; n = 12) 52,560 +/- 6,730 (p less than 0.005). Parietal cells/mg wet weight gastric mucosa: 1,910 +/- 490 (C), 1,980 +/- 140 (GI), 1,700 +/- 200 (GII), 1,170 +/- 220 (GIII, p less than 0.025), 2,580 +/- 240 (DU, p less than 0.05), 1,690 +/- 150 (GU), 1,500 +/- 250 (BI), 1,360 +/- 320 (BII). Parietal cell concentration (density) did not differ in males and females and did not change with age. The method delivers relevant cell numbers, is suitable to detect qualitative differences and can be used for the interpretation of biochemical studies.
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PMID:Morphologically different biopsy specimens of the human gastric mucosa. I. The use of enzymatic cell isolation for quantitative determination of parietal cells. 301 1

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

An association between eosinophils and tissue damage has been observed in numerous disorders. However, few reports have addressed the role of infiltrating eosinophils in gastric ulcer healing. The aim of this study was to investigate the kinetics and role of eosinophils infiltrating experimental chronic gastric ulcers in the rat. We developed a monoclonal antibody against human matrix metalloproteinase 1 (MMP1) purified from conditioned culture medium of human skin fibroblasts. Acetic acid-induced gastric ulcers were resected from rats on days 1, 3, 5, 10, 20, 40, and 180 after the days of induction (day 0). Tissue specimens were immunostained with this antibody and examined with an electron microscope. Few eosinophils were observed in the granulation tissue until day 20. By days 40 and 180, MMP1-positive eosinophils had increased in the granulation tissue of open ulcers. Azan staining revealed dispersed collagen fibers around infiltrating eosinophils. In contrast, scars demonstrated few eosinophils in fibrous tissue on days 40 and 180. Eosinophils which express MMP1 infiltrate granulation tissue at the chronic stage of gastric ulceration. The results suggest that eosinophils may play a role in tissue remodeling and deterioration of ulceration.
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PMID:Kinetics and collagenolytic role of eosinophils in chronic gastric ulcer in the rat. 937 22

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

Severe intracerebral hemorrhage (ICH) produces gastric pathology in about 30% of the patient population, even after the standard treatment of H2 receptor blockers or proton pump inhibitors. This study was undertaken to establish a rat model of ICH-induced gastric ulcer. Adult male Sprague-Dawley rats (300-350 g) were divided into two hemorrhage groups and a sham control group. ICH was produced either by injection of 100 microl of autologous arterial blood or by injection of 4 microl saline containing 0.6 unit of bacterial collagenase VII into the right basal ganglia. Rats were sacrificed at 24, 48, 72 h, and 7 days after ICH to harvest brains and stomachs. Greater degrees of hemorrhage and brain edema were observed in collagenase-induced ICH. Motor behavior decreased significantly after 24 h in both models. The incidence of acute ulceration with destruction of the forestomach epithelium was extremely low at 8.7% in the collagenase injection model and 4.8% in the blood injection rats. Small, pinpoint hemorrhages (petechiae) were noticed in 38% of rats after blood injection and 22% after collagenase injection, in the glandular portion of the gastric mucosa with penetration of red blood cells and inflammatory cells into the gastric mucosa. Enhanced tumor necrosis factor alpha (TNFalpha) and cyclooxygenase 2 (COX-2) expressions were observed in gastric tissues after ICH with more intense staining occurring at 24 and 48 h. Due to the low incidence of ulceration, ICH-induced gastric ulceration in rodents may not appropriate for evaluating the potential human risk of gastric ulceration after ICH.
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PMID:Acute gastric changes after intracerebral hemorrhage in rats. 1575 35