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 tissue-type plasminogen activator (t-PA) was investigated in the gastric ulcer formation induced by microvascular derangement. The rat stomach was exposed and repeated electrical stimuli (irritation) were applied on the small arterial wall close to the lesser curvature to induce mucosal ischemia followed by hyperemia. The t-PA activity in the regional blood of the stomach was significantly elevated as early as 5 min after the irritation. Immunohistochemical study using anti-t-PA monoclonal antibody revealed that t-PA was detectable in the endothelial cells of capillaries and collecting venules, suggesting the involvement of endothelium-mediated fibrinolytic activity in the irritation-induced ulcer formation. Pretreatment of SOD or allopurinol significantly attenuated the irritation-induced t-PA activation, suggesting that the t-PA activity was modulated by xanthine oxidase-associated superoxide anions. CV-6209, a selective antagonist of platelet-activating factor (PAF), also prevented the activation of t-PA as well as ulcer formation, providing a concept that PAF may be associated with the local fibrinolytic activation which may cause hemorrhagic changes in the gastric mucosal microvasculature. The present study supports the hypothesis that increased t-PA activity may reflect the microvascular endothelial damages caused by vasomotor derangement and suggests that oxygen-derived free radicals may participate in the regulation of endothelium-derived fibrinolytic activities in the mucosal microvasculature.
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PMID:Involvement of superoxide anion and platelet-activating factor in increased tissue-type plasminogen activator during rat gastric microvascular damages. 165 Sep 66

Diethyldithiocarbamate (DDC) was injected subcutaneously in the rat and the mechanism of gastric ulcer formation was investigated. DDC induced gastric ulcers in a dose-dependent manner. DDC significantly suppressed gastric mucosal copper-zinc superoxide dismutase (Cu, Zn-SOD) activity at 2 hr. However, manganese-superoxide dismutase (Mn-SOD) activity was not changed. Gastric mucosal blood flow (GMBF) decreased to 52% of the control level at 2 hr after administration of DDC and gradually increased to reach the control level by 7 hr. A Shay rat preparation (4 hr) was used to study gastric secretion. DDC (200, 400 and 800 mg/kg) inhibited acid secretion to about 80% of the control level. Histopathological examination of the gastric mucosa after administration of DDC revealed mucosal congestive findings from 1 hr to 3 hr. These data suggested that the mechanism of DDC-induced gastric ulcer formation may be attributable to a decreased level of GMBF and O2- production owing to decreased SOD activity.
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PMID:Mechanism of diethyldithiocarbamate-induced gastric ulcer formation in the rat. 215 49

Peroxidative tissue damage has been reported to contribute to several pathological disorders. Despite high exposure to both exogenous and endogenous oxidant stress, the strong cell defence mechanism of the gastric mucosa protects mucosal epithelial cells against these noxious stimuli. However, some environmental factors involved in lipid peroxidation (such as cadmium), which disrupt gastric mucosal protection, may impair the mucosal barrier and facilitate the occurrence of gastric ulcers. In an experimental study to investigate this hypothesis, the level of cadmium-induced lipid peroxidation products (TBARS) and an antioxidant enzyme (SOD) were investigated. The mucin content (P < 0.01) and prostaglandin levels (P < 0.05) of mucosa as components of the gastric mucosal barrier were found to be significantly reduced in rats exposed to 15 ppm of cadmium in water for 30 days when compared with those of unexposed controls. TBARS levels in blood (P < 0.05) and mucosa (P < 0.001) increased markedly in cadmium-exposed animals whereas blood SOD levels remained unchanged. The significant correlation between TBARS and mucosal cadmium (r = 0.664, P < 0.01), as well as between cadmium and PGE2 (r = -0.719, P < 0.01), led to the conclusion that cadmium-induced lipid peroxidation is involved in the increased vulnerability of gastric mucosa to injurious stimuli in rats. This susceptibility may be responsible for the high incidence of stress-induced gastric ulcer in the population.
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PMID:Role of lipid peroxidation in cadmium-induced impairment of the gastric mucosal barrier. 792 76

We developed a new gastric ulcer model in which the ulcers are induced by the local injection of a ferrous iron and ascorbic acid (Fe/ASA) solution into the gastric wall. These ulcers resemble human gastric ulcers that penetrate the muscularis mucosa. The involvement of oxygen radical-mediated lipid peroxidation as the cause of these ulcers was investigated. With ferrous iron or ascorbic acid alone, gastric ulcers did not form, whereas penetrating ulcers were produced by the simultaneous injection of the Fe/ASA solution in a dose-dependent manner. Lipid peroxides significantly accumulated in the gastric mucosa from 1 to 24 h after the injection of the Fe/ASA solution. This increase in lipid peroxides preceded grossly evident gastric ulcer. Treatment with superoxide dismutase (SOD, recombinant human CuZnSOD) significantly reduced the size of the ulcers and inhibited the accumulation in lipid peroxides in the gastric mucosa, while treatment with apo-SOD or heat-inactivated SOD did not. These results suggest that lipid peroxidation mediated by oxygen radicals plays a crucial role in the pathogenesis of the gastric ulceration induced by the Fe/ASA solution.
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PMID:A new gastric ulcer model in rats produced by ferrous iron and ascorbic acid injection. 853 16

Many factors, such as the selection of acupoints, the interval between acupunctures, the acupuncture time, the manipulation and the specification of acupuncture needles, are capable of affecting curative effects. There were some studies on these factors ago. However each of these studies only related to a single factor. These studies could not reflect the clinical truth, and could not provide accurate overall data for medical staff. In order to solve the above problems, we carried out an animal experiment designed by L9 (3(4)) orthogonal design. The experiment which consisted of 9 acupuncture groups and 3 control ones was carried out in 108 rats, which were suffered from experimental gastric ulcer. In the experiment, the body weight, ulcer area, plasma SOD and LPO of each rat were observed. The results showed that in the acupuncture treatments for experimental gastric ulcer in rats, 10 minutes' electric acupuncture treatment using thinner needles and the method that each rat was treated every other day were the best methods. The reason why the above results came into being was elucidated in this paper.
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PMID:[A study on factors of acupuncture methods affecting effects through acupuncture treatments for experimental gastric ulcer in rats]. 870 69

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

The objective of the present study is to delineate the mechanism of oxidative damage in human gastric ulcerated mucosa despite the presence of some antioxidant enzymes. We report for the first time the critical role of an endogenous peroxidase, a major H(2)O(2) metabolizing enzyme, in controlling oxidative damage in gastric mucosa. Human gastric mucosa contains a highly active peroxidase in addition to the myeloperoxidase contributed by neutrophil. In both non-Helicobacter pylori (H. pylori)- and H. pylori-mediated gastric ulcer, when myeloperoxidase level increases due to neutrophil accumulation, gastric peroxidase (GPO) level decreases significantly. Moreover, gastric ulcer is associated with oxidative damage of the mucosa as evidenced by significant increase in lipid peroxidation, protein oxidation, and thiol depletion indicating accumulation of reactive oxygen metabolites (ROM). Mucosal total superoxide dismutase (Mn and Cu-Zn SOD) level also decreases significantly leading to increased accumulation of O(2)(*-). To investigate the plausible ROM-mediated inactivation of the GPO during ulceration, the enzyme was partially purified from the mucosa. When exposed to an in vitro ROM generating system, using Cu(2+), ascorbate, and H(2)O(2,) the enzyme gets inactivated, which is dependent on Cu(2+), ascorbate, or H(2)O(2). Insensitivity to SOD excludes inactivation by O(2)(*-). However, complete protection by catalase indicates that H(2)O(2) is essential for inactivation. Sensitivity to EDTA and hydroxyl radical *OH) scavengers indicates that GPO is inactivated most probably by *OH generated from H(2)O(2). We propose that GPO is inactivated in vivo by ROM generated by activated neutrophil. This leads to further accumulation of endogenous H(2)O(2) to cause more oxidative damage to aggravate the ulcer.
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PMID:Critical role of an endogenous gastric peroxidase in controlling oxidative damage in H. pylori-mediated and nonmediated gastric ulcer. 1193 99

The ulcer protective potential of methanolic extract of Emblica officinalis Gaertn. (EOE) was assessed in different acute gastric ulcer models in rats induced by aspirin, ethanol, cold restraint stress and pyloric ligation and healing effect in chronic gastric ulcers induced by acetic acid in rats. EOE, 10-50 mg/kg administered orally, twice daily for 5 days showed dose-dependent ulcer protective effects in all the above acute ulcer models (36.0-98.3% protection, P < 0.2 to P < 0.001) and significant ulcer healing effect in dose of 20 mg/kg after 5 (control ulcer index: 20.2+/-2.3 mm(2)/rat, % healing 59.6%, P < 0.001) and 10 (control UI: 11.0+/-1.7, % healing 65.5%, P < 0.01) days treatment. Further study on gastric mucosal factors showed that it significantly decreased the offensive factors like acid (acid output-control 118.7+/-12.1 microEq/4 h, EOE% decrease 65.9%, P < 0.01) and pepsin (peptic output-control 738.8 micromol/4 h, EOE% decrease 46.2%, P < 0.001) and increased the defensive factors like mucin secretion (TC:P ratio-control 1.21+/-0.15, EOE% increase 95.0%, P < 0.01), cellular mucus (TC:P ratio-control 1.16+/-0.13, EOE% increase 53.4%, P < 0.05) and life span of mucosal cells (DNA content of gastric juice-control 77.3+/-8.7 microg/m per 100 g body weight, EOE% decrease 42.1%, P < 0.05). EOE showed significant antioxidant effect in stressed animals (control UI 35.8+/-2.5, antioxidant status: LPO 0.58+/-0.03 nmol MDA/mg protein, SOD and CAT 227.8+/-6.3 and 18.4+/-1.2 U/mg protein respectively; EOE% decrease in UI 88.2%, mucosal LPO 69.0%, SOD 53.1% and increase in mucosal CAT 59.8%, P < 0.001 respectively) and did not have any effect on cell proliferation in terms of DNA microg/mg protein or glandular weight. The results showed that EOE had significant ulcer protective and healing effects and this might be due to its effects both on offensive and defensive mucosal factors.
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PMID:Antiulcerogenic effect of methanolic extract of Emblica officinalis: an experimental study. 1216 98

This study is to investigate therapeutic effect of astaxanthin on acetic acid-induced gastric ulcer in rats. Rats were divided into control group, ulcer control group, and astaxanthin (5, 10, and 25 mg x kg(-1)) groups at random, 8 rats in each group. After administered for 10 days consecutively, all the rats were sacrificed. The area of ulcer and the levels of MDA, SOD, CAT and GSH-Px in gastric mucosa were measured. Compared with ulcer control group, in astaxanthin (5, 10, and 25 mg x kg(-1)) groups, the area of ulcer was decreased significantly. Level of MDA decreased while activities of SOD, CAT and GSH-Px increased (P < 0.05). Astaxanthin has good therapeutic effect on acetic acid-induced gastric ulcer in rats. Eliminating free radical and improving local blood circulation of the ulcer may be the mechanism of action.
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PMID:[Therapeutic effect of astaxanthin on acetic acid-induced gastric ulcer in rats]. 1961 36

The ethanol leaf extract (ELE) of Cassia fistula Linn. (Caesalpinaceae) was evaluated for antiulcer activity against pylorus ligation-induced gastric ulcer. Ranitidine (30 mg/kg b.w.) and ELE at doses of 250, 500, and 750 mg/kg b.w. were administered orally in different groups of rats (n = 6), 1 h prior to pyloric ligation. Four hours after pyloric ligation, the gastric juice was collected for evaluation of various parameters. The antiulcer activity of ELE was evidenced by the significant attenuation of gastric volume, pH, free acidity, and total acidity in the gastric juice of pyloric-ligated rats in a dose-dependent manner, and this protective effect could be due to strengthening of the mucosal defense mechanism. ELE pre-treatment significantly attenuated the fall in status of sialic acid and fucose accompanied by an increase in hexose, hexosamine, total non-amino polysaccharide, total carbohydrate, and C:P ratio in the gastric juice of pylorus-ligated rats, and this effect could be due to protection of the mucosal barrier system. ELE pre-treatment significantly prevented the increase in LPO and SOD accompanied by a fall in CAT, in the gastric juice of pyloric-ligated rats. This protective ability of ELE against pylorus ligation-induced gastric ulcer could be attributed to its free radical scavenging and antioxidant properties. Higher doses of ELE (750 mg/kg b.w.) produced maximum antiulcer activity comparable to ranitidine treatment. In essence, the antiulcer activity of ELE could be attributed to (i) a decrease in gastric acid secretion, (ii) protection of the mucosal barrier and restoration of mucosal secretions, (iii) inhibition of free radical generation or prevention of lipid peroxidation, and (iv) free radical scavenging or antioxidant properties.
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PMID:Antiulcer activity of ethanol leaf extract of Cassia fistula. 2067 73


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