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 evaluate whether bombesin treatment has a facilitatory effect on the healing of chronic gastric ulcer, following the induction of ulcer by serosal application of acetic acid, rats were given bombesin (30 microg/kg/day; subcutaneously) or vehicle three times a day for 7, 14 or 21 days until they were decapitated. Neither food intake nor gastric emptying rate in either vehicle-treated or bombesin-treated groups was not statistically different from control rats. Similarly, ulcer indices and gastric myeloperoxidase (MPO) activities at the first and second weeks of injury were not different among the groups. However, in the 3-week ulcer group, bombesin treatment reduced tissue MPO level significantly back to control levels. Moreover, the analysis of the surface epithelium by scanning electron and light microscopy demonstrated a significant reduction in the severity of ulcers by bombesin treatment. Pretreatment with CCK antagonists (L-364,718 or L365,260; 25 micromol/kg/day) before bombesin treatment showed that neither of the CCK antagonists had a significant effect on the bombesin-mediated healing process, suggesting that CCK receptors are not involved in the action of bombesin. In accordance with the previous studies that show its acute gastroprotective effects, bombesin is also effective in promoting the healing process of chronic gastric ulcer in rats.
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PMID:Healing-promoting effect of bombesin treatment on chronic gastric ulcer in rats. 1204 14

In this study, we examined the effect of rebamipide, a mucoprotective drug, on gastric ulcer healing in Mongolian gerbils infected with H. pylori. Male Mongolian gerbils were inoculated with H. pylori or vehicle alone 12 hr after the production of an acetic acid-induced gastric ulcer. On day 5, the gerbils inoculated with H. pylori were divided into three groups and fed rebamipide-containing diet (0.038%, 60 mg/kg, or 0.0038%, 6 mg/kg), or standard laboratory chow. The gerbils inoculated with the vehicle were fed standard laboratory chow throughout the experiment. The gerbils were killed on day 5, 15, or 30 after ulcer production, and removed stomachs were subjected to calculation of ulcer size, culture for H. pylori, and measurement of myeloperoxidase activity, a marker for neutrophil infiltration, in ulcerated tissue. Apoptotic and proliferating cells of gastric epithelium in ulcer margins were detected by the in situ DNA nick end-labeling method and immunohistochemical staining for 5-bromo-2'-deoxyuridine (BrdU), respectively. Rebamipide did not affect colonization levels of H. pylori. Infection with H. pylori did not affect ulcer size by day 5 but significantly delayed ulcer healing by days 15 and 30, accompanied by an increase in the number of apoptotic cells, a decrease in the number of BrdU-positive cells, and an increase in myeloperoxydase activity. Rebamipide prevented delay of ulcer healing and abolished these effects of H. pylori on cell kinetics and neutrophil infiltration. In conclusion, rebamipide may prevent the delay of acetic acid-induced gastric ulcer healing caused by H. pylori through modulating cell kinetics and inhibiting neutrophil infiltration.
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PMID:Rebamipide prevents delay of acetic acid-induced gastric ulcer healing caused by Helicobacter pylori infection in Mongolian gerbils. 1214 20

Bombesin has been shown to have trophic effects on the gastrointestinal tissue. Bombesin has direct mitogenic effects besides stimulating release of gastric hormones. The aim of this study was to investigate the effect of bombesin in hemorrhagic shock-induced stress ulcers in rats, and the role of cholecystokinin (CCK) receptors in this activity. Hemorrhagic shock was created by withdrawing 3 ml blood/200 g b.w. of rats. At the end of the 1-hour hypovolemic shock period, histological analysis, gastric ulcer index, gastric myeloperoxidase activity and gastric protein oxidation levels were determined. When given before the hemorrhage, subcutaneous bombesin (10 microg/kg) reduced macroscopically gastric ulcer index (p < 0.05). Blockade of CCK-A receptors with intraperitoneal MK-329 (1 mg/kg) did not reverse bombesin-induced gastroprotection. Blockade of CCK-B receptors with intraperitoneal L-365,260 (25 mg/kg) reversed bombesin-induced gastroprotection. Blockade of the two receptors resulted in no gastroprotection at all. It is concluded that bombesin treatment attenuated hemorrhagic shock-induced stress ulcers in rats via CCK receptors.
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PMID:Role of bombesin and cholecystokinin receptors in gastric injury induced by hemorrhagic shock in the rat. 1271 34

This investigation was undertaken to study the effect of methimazole (MMI) on gastric acid secretion and stress and chemically induced gastric ulcer in rats. Acid secretion studies were undertaken using pylorus-ligated rats pretreated with MMI (10-100 mg/kg, i.p.). The effect of orally administered MMI on water-immersion restraint (WIR) stress, indomethacin and ethanol-induced gastric ulcers was also tested. The level of myeloperoxidase (MPO), non-protein sulfhydryls (NP-SH) and gastric wall mucus was measured in the glandular stomach of rats following ethanol-induced gastric lesions. There was a dose-dependent inhibition of gastric acid secretion and ulcerogen induced gastric lesion formation in the MMI treated rats. Our morphological and histological studies showed a complete prevention of ethanol-induced lesions in the rats treated with high dose (100 mg/kg) of MMI. A significant attenuation of ethanol-induced increase in gastric MPO activity, depletion of NP-SH and reduction of gastric wall mucus was also observed in MMI treated rats. These findings clearly suggest the involvement of endogenous pro-inflammatory agents and oxidative stress in mediating the gastroprotective effect of MMI.
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PMID:Methimazole prevents stress and chemical induced gastropathy in rats. 1470 74

To evaluate the role of estrogen treatment on the healing of acetic acid-induced gastric or colonic injury, rats were given 17beta estradiol benzoate (0.001, 0.1, and 10 mg/kg) or vehicle for 7 days (following the induction of ulcer) or 4 days (following the induction of colitis) until they were decapitated. Food intake and fecal output were decreased by estradiol treatment but gastric emptying rate was not changed. Estradiol (10 mg/kg) reduced gastric ulcer index and colonic damage score compared to vehicle-treated groups. SEM and light microscopy demonstrated a significant reduction in the severity of ulcers and colitis by estradiol treatment. Gastric microscopic score was not changed by estradiol treatment, whereas in the colonic tissue score was significantly reduced. Elevated gastric MPO levels were reduced in gastric but not in colonic tissues as compared with corresponding vehicle groups. In conclusion, exogenous estradiol treatment at pharmacological doses improves the healing of both gastric and colonic injury induced by acetic acid in rats.
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PMID:Estradiol treatment ameliorates acetic acid-induced gastric and colonic injuries in rats. 1476 Sep 43

TNF-alpha has numerous biological activities, including the induction of chemokine expression, and is involved in many gastric injuries. C-C chemokines [monocyte chemotactic protein (MCP)-1 and macrophage inflammatory protein (MIP)-1alpha] and C-X-C chemokines [MIP-2 and cytokine-induced neutrophil chemoattractant (CINC)-2alpha] mediate chemotaxis of monocytes and neutrophils, respectively. We examined the roles of TNF-alpha and dynamics of chemokine expression in gastric ulceration including ulcer recurrence and indomethacin-induced injury. Rats with healed chronic gastric ulcers received intraperitoneal TNF-alpha to induce ulcer recurrence. Some rats were given neutralizing antibodies against neutrophils or MCP-1 together with TNF-alpha. In a separate experiment, rats were orally administered 20 mg/kg indomethacin with or without pretreatment with pentoxifylline (an inhibitor of TNF-alpha synthesis) or anti-MCP-1 antibody. TNF-alpha (1 microg/kg) induced gastric ulcer recurrence after 48 h, which was completely prevented by anti-neutrophil antibody. TNF-alpha increased the number of macrophages and MCP-1 mRNA expression in scarred mucosa from 4 h, whereas it increased MPO activities (marker of neutrophil infiltration) and mRNA expression of MIP-2 and CINC-2alpha from 24 h. Anti-MCP-1 antibody inhibited leukocyte infiltration with reduction of the levels of C-X-C chemokines and prevented ulcer recurrence. Indomethacin treatment increased TNF-alpha/chemokine mRNA expression from 30 min and induced macroscopic erosions after 4 h. Pentoxifylline inhibited the indomethacin-induced gastric injury with reduction of neutrophil infiltration and expression of chemokine (MCP-1, MIP-2, and CINC-2alpha). Anti-MCP-1 antibody also inhibited the injury and these inflammatory responses but did not affect TNF-alpha mRNA expression. In conclusion, increased MCP-1 triggered by TNF-alpha may play a key role in gastric ulceration by regulating leukocyte recruitment and chemokine expression.
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PMID:Monocyte chemotactic protein-1 regulates leukocyte recruitment during gastric ulcer recurrence induced by tumor necrosis factor-alpha. 1520 18

Recent studies clearly suggest a role of central nervous system in regulation of gastrointestinal function and defense against ulcerogens. In the present study, attempt was made to investigate the effect of centrophenoxine (CPH), a nootropic drug on gastric acid secretion and experimentally induced gastric ulcer in rats. Acid secretion studies were undertaken using pylorus-ligated rats pretreated with CPH (10-100 mg/kg, i.p.). The effect of orally administered CPH on water-immersion restraint (WIR) stress, indomethacin and ethanol-induced gastric ulcers was also examined. The level of myeloperoxidase (MPO), non-protein sulfhydryls (NP-SH) and gastric wall mucus was measured in the glandular stomach of rats following ethanol-induced gastric lesions. There was a dose-dependent inhibition of gastric acid secretion in the CPH treated rats. Pretreatment with CPH significantly protected gastric mucosa against ethanol and indomethacin induced gastric lesion. Only low dose of CPH (30 mg/kg) was found to be effective against stress ulcers. A significant attenuation of ethanol-induced increase in gastric MPO activity, depletion of NP-SH and reduction of gastric wall mucus was also observed in CPH treated rats. These findings clearly suggest the involvement of endogenous pro-inflammatory mediators and oxidative stress in mediating the gastroprotective effect of CPH.
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PMID:Effect of centrophenoxine on water-immersion restraint stress- and chemically-induced gastric ulcers in rats. 1568 6

Previous studies have shown a definite role of mitogen activated protein kinase (MAPK) and epidermal growth factors (EGF) in the maintenance and repair of gastric mucosa. The aim of this study is to investigate the effect of menadione, an activator of MAPK pathway, on gastric acid secretion and experimentally induced gastric ulcer in rats. Acid secretion studies were undertaken using pylorus-ligated rats pretreated with menadione (5 - 45 mg/kg, i.p.). The effect of orally administered menadione on ethanol-induced gastric ulcers was also examined. The level of gastric wall mucus, non-protein sulfhydryls (NP-SH) and myeloperoxidase (MPO) was measured in the glandular stomach of rats following ethanol-induced gastric lesions. There was a significant inhibition of gastric acid secretion in the menadione treated rats. Pretreatment of rats with menadione significantly protected gastric mucosa against ethanol-induced gastric lesion. A significant attenuation of ethanol-induced reduction of gastric wall mucus, depletion of NP-SH and increase in gastric MPO activity was also observed in menadione treated rats. In conclusion, this study clearly showed acid antisecretory and antiulcer activity of menadione. Further studies are warranted to determine the mechanism of antiacid and gastroprotective effect of menadione.
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PMID:Menadione protects gastric mucosa against ethanol-induced ulcers. 1594 79

Prostaglandin, a key molecule that stimulates the complex array of ulcer healing mechanism, gets synthesized in the mucosal cells by cyclooxygenase (COX) enzymes: COX-1 and COX-2. High expression level of COX-2 protein at healing ulcer margins highlights its role in ulcer healing and hypothesized to be an important contributing factor in healing mechanism of anti-ulcer drugs. In the present study we have compared the expression profile of COX-2 protein, prostaglandin E2 (PGE2) levels and myeloperoxidase activity in acetic acid induced chronic gastric ulcer model in rats treated with omeprazole, misoprostol and COX-2 selective nonsteroidal anti-inflammatory drug (NSAID) celecoxib. Both COX-2 expression and PGE2 level have shown differential pattern in different treated groups parallel to the differential effects of these drugs on ulcer healing. Omeprazole has significantly elevated the expression level of COX-2 protein, PGE2 level (19.37%), and decreased myeloperoxidase activity (81.92%), thereby causing the most effective ulcer healing (89.74%). Similar trend was observed with misoprostol, but with relatively less pronounced ulcer healing and COX-2 expression. Celecoxib has retarded COX-2 expression and delayed ulcer healing. Therefore, induction of COX-2 expression leading to higher level of prostaglandin appears to be an important contributing factor in drug mediated ulcer healing apart from the respective mechanisms of different drugs.
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PMID:Cyclo-oxygenase-2 expression and prostaglandin E2 production in experimental chronic gastric ulcer healing. 1613 65

Usnea longissima, a medicinal lichen of Anatolia (Turkey), is used in the treatment of gastric ulcer in local folk medicine. In this paper, the gastroprotective effect of usnic acid (UA) isolated from Usnea longissima was investigated in the indomethacin-induced gastric ulcers in rats at doses of 25, 50, 100 and 200 mg/kg body weight. The gastric lesions were significantly reduced by all doses of UA as compared with the indomethacin (25 mg/kg body weight) treated group. In the stomach tissues of treated animals, the in vivo antioxidant levels were evaluated. The administration of indomethacin caused a significant decrease in the levels of superoxide dismutase (SOD), glutathione peroxidase (GPx) and reduced glutathione (GSH), and an increase in the lipid peroxidation (LPO) level (p < 0.05). The administration of all doses of UA reversed the trend, inducing a significant increase of SOD, GSH and GPx levels and a reduction in LPO level in tissues. However, catalase (CAT), glutathione reductase (GR) and myeloperoxidase (MPx) activities, increased by indomethacin, were found to be lower in the UA- and ranitidine-treated groups. The gastric mucosal constitutive NO synthase (cNOS) and inducible NO synthase (iNOS) activities were also investigated in tissues of UA- (100 mg/kg), ranitidine- (50 mg/kg) and indomethacin-treated rat groups. The administration of UA and ranitidine increased the cNOS activity and lowered the iNOS activity as compared with indomethacin-treated group. These results suggest that the gastroprotective effect of UA can be attributed to its reducing effect on the oxidative damage and neutrophil infiltration in tissues.
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PMID:Gastroprotective and antioxidant effects of usnic acid on indomethacin-induced gastric ulcer in rats. 1616 75


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