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  • 1
    Electronic Resource
    Electronic Resource
    Lansoprazole promotes gastric mucosal cell proliferation and migration by activating p44/p42 mitogen-activated protein kinase (2004)
    Oxford, UK; Malden , USA : Blackwell Science Inc
    Wound repair and regeneration 12 (2004), S. 0 
    Details
    ISSN: 1524-475X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Cell proliferation and migration are important repair mechanisms in cell defect type mucosal injuries, such as peptic ulcers. To evaluate the level of cell restitution in vitro, we established a normalized assay system for analyzing the area of a tissue defect created in the center of a cultured cell layer. Although proton pump inhibitors are known to be potently effective in the treatment of peptic ulcers by inducing acid suppression, they are also effective in low-acid conditions, such as in gastric ulcers associated with severe atrophic gastritis of the corpus. The present study was designed to examine the pH-independent effect of lansoprazole (LPZ) on cell restitution in vitro. The mouse gastric mucosal cell line, GSM06, was cultured to confluence. A 4-fluoric ethylene-tipped aluminum stick was then used to produce a cell-free area in the center of the culture well. After measuring the area of the cell defect using a digital analyzer equipped with an inverted microscope, LPZ was added to each well; the area of the residual cell defect was then measured 6 and 24 hours after LPZ administration. To investigate the involvement of the p44/p42 mitogen-activated protein kinase (MAPK) and p38 MAPK in this process, PD98059 (a MEK inhibitor) or FR167653 (a p38 MAPK inhibitor) was added to the cell cultures. In a separate experiment, GSM06 cells were cultured to the subconfluent level, each test agent was added, and the cell number in each well was measured using an MTT assay 16 hours after the administration of the agents. Six hours after the addition of LPZ, a slight but significant increase in the cell restitution rate was observed in the LPZ-treated groups compared with that in the control group. After 24 hours, a further significant increase in the cell restitution rate was observed in the LPZ groups compared with that in the control group. While the addition of PD98059 significantly attenuated the cell restitution rate in the LPZ groups, the addition of FR167653 had no such effect. The total cell number in the subconfluent cell cultures was significantly increased in the LPZ-treated groups compared with that in the control group. In conclusion, LPZ promotes the healing of injured gastric mucosal cells following injury by enhancing cell proliferation and migration. Furthermore, the mechanism by which cell proliferation and migration is promoted by LPZ may involve the activation of p44/p42 MAPK.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1067-1927.2004.012116.x
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  • 2
    Electronic Resource
    Electronic Resource
    Melanoidin, a Food Protein-Derived Advanced Maillard Reaction Product, Suppresses Helicobacter pylori in vitro and in vivo (2004)
    Oxford, UK : Blackwell Science Ltd
    Helicobacter 9 (2004), S. 0 
    Details
    ISSN: 1523-5378
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background.  Extracellular urease proteins located on the surface of Helicobacter pylori are gastric mucin-targeted adhesins, which play an important role in infection and colonization to the host. In this study we have determined the inhibitory activity of a variety of melanoidins, protein-derived advanced Maillard reaction products, ubiquitously found in heat-treated foods, on urease-gastric mucin adhesion. In addition, we have determined the anticolonization effect of melanoidin I, prepared by the Maillard reaction between casein and lactose, in an animal model and in human subjects infected with this bacterium.Methods.  The inhibitory activity of each compound was determined by a competitive binding assay of labeled gastric mucin to plate-immobilized urease. Melanoidin I was used in an in vivo trial using euthymic hairless mice as an infection model. Melanoidin I was consumed for 8 weeks by subjects infected with H. pylori. The [13C] urease breath test and H. pylori-specific antigen in the stool (HpSA) test were performed on subjects at week 0 and week 8.Results.  A variety of food protein-derived melanoidins strongly inhibited urease-gastric mucin adhesion in the concentration range of 10 µg/ml to 100 µg/ml. In particular, melanoidin I significantly (p 〈 .05) suppressed colonization of H. pylori in mice when given for 10 weeks via the diets. Eight weeks daily intake of 3 g melanoidin I significantly (p 〈 .05) decreased the optical density of HpSA in subjects.Conclusion.  Foods containing protein-derived melanoidins may be an alternative to antibiotic-based therapy to prevent H. pylori that combines safety, ease of administration and efficacy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1083-4389.2004.00263.x
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  • 3
    Electronic Resource
    Electronic Resource
    Catalase and Superoxide Dismutase Secreted from Helicobacter pylori (1997)
    Cambridge, MA, USA : Blackwell Science, Inc.
    Helicobacter 2 (1997), S. 0 
    Details
    ISSN: 1523-5378
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Previously, we have reported that toxic oxidants produced by activated neutrophils play a pivotal role in the development of Helicobacter pylori–induced gastric mucosal damage. Microorganisms, however, are characterized by their ability to produce a variety of antioxidant enzymes. This study is designed to measure the oxygen radical scavenging enzymes, such as catalase and superoxide dismutase (SOD), and urease in the supernatant of H. pylori (NCTC11637) suspension.〈section xml:id="abs1-2"〉〈title type="main"〉Materials and Methods. H. pylori was inoculated on a sheep blood agar plate and harvested. Bacterial suspensions (109 cfu/ml phosphate buffer) were washed twice and incubated at 37°C for 1, 2, 12, and 24 hours or were sonicated in ice. Their supernatants were obtained by centrifugation and filtration. SOD activity was measured spectrophotometrically by the cytochrome c method. Catalase activity was assayed by the fall in absorbance at 240 nm as H2O2 is degraded. Urease activity was determined by measuring the release of ammonia using Berthelot reaction.〈section xml:id="abs1-3"〉〈title type="main"〉Results.Activities of both SOD and catalase were detected in the supernatants of 1-hour microaerophilic incubation. Their activities were almost constant in 4-, 12-, and 24-hour microaerobic incubation or sonication. Urease activity was increased dramatically in proportion to the period of microaerobic incubation.〈section xml:id="abs1-4"〉〈title type="main"〉Conclusion.Although H. pylori possesses antioxidant as a constitutive compartment, the magnitude of its secretion was below the detectable level. It is not likely that SOD and catalase play a significant role for scavenging the oxidants from injured gastric mucosa, such as infiltrated leukocytes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1523-5378.1997.tb00067.x
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  • 4
    Electronic Resource
    Electronic Resource
    Decreased gastric mucosal barrier function in diabetes mellitus (1999)
    Springer
    Journal of gastroenterology 34 (1999), S. 288-291 
    Details
    ISSN: 1435-5922
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s005350050260
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  • 5
    Electronic Resource
    Electronic Resource
    Malabsorption of long-chain fatty acid in cholera toxin-induced secretory diarrhea (1986)
    Springer
    Digestive diseases and sciences 31 (1986), S. 519-523 
    Details
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of cholera toxin-induced diarrhea on the absorption of fatty acids of different chain lengths were investigated using rat small intestine. In the study using isolated jejunal loops, the absorption of the long-chain fatty acid, linoleic acid, into the intestinal mucosa was significantly impaired 90 min after the administration of linoleic acid micelles in the cholera toxin-treated rats. This reduction of linoleic acid absorption in the cholera toxin-treated rats was not found at 180 min. We could not find any mucosal accumulation of labeled linoleic acid or disturbance of triglyceride formation in the intestinal mucosa as compared with that of controls. The amount of linoleic acid transported into the intestinal lymph was delayed and reduced in cholera toxin-treated rats. Furthermore, the absorption of the medium-chain-length fatty acid, octanoic acid, was unchanged in the cholera toxin-treated rats. These results suggest that intestinal secretion induced by cholera toxin may delay the mucosal uptake and lymphatic transport of long-chain fatty acids. Cholera toxin may not affect triglyceride formation in the epithelial cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01320318
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  • 6
    Electronic Resource
    Electronic Resource
    Identification of proline-specific carboxypeptidase localized to brush border membrane of rat small intestine and its possible role in protein digestion (1989)
    Springer
    Digestive diseases and sciences 34 (1989), S. 400-406 
    Details
    ISSN: 1573-2568
    Keywords: small intestine ; brush border membrane ; carboxypeptidase P
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A proline-specific carboxypeptidase (carboxypeptidase P, EC 3.4.12.-) was identified and partially characterized in the brush border membrane fraction of rat intestinal enterocytes and shown to be distinct from pancreatic proteases. The carboxypeptidase activity of isolated brush border membranes, with Z-Gly-Pro-Leu as substrate, was 43 nmol/min/mg protein representing a 16-fold purification when compared with mucosal cell homogenates. Activity was maximal in the middle region of the small intestine, and villus cells had twice the activity of crypt cells. Carboxypeptidase activity was maximal at pH 7.0, was stimulated by divalent cations, and was inhibited by metal chelating agents, suggesting that it is a metalloenzyme. The enzyme had the highest activity with synthetic peptides containing proline penultimate to the carboxy terminus. In vivopatterns of hydrolysis and absorption of amino acids from Z-Pro-Trp were examined using an intestinal perfusion technique. These studies indicate that brush border membrane carboxypeptidase may play an important role in the digestion of prolinecontaining peptides and proteins.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01536262
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  • 7
    Electronic Resource
    Electronic Resource
    IL-1 is an important mediator for microcirculatory changes in endotoxin-induced intestinal mucosal damage (1996)
    Springer
    Digestive diseases and sciences 41 (1996), S. 2482-2492 
    Details
    ISSN: 1573-2568
    Keywords: interleukin-1 ; endotoxin ; microcirculatory disturbance ; intestinal mucosal damage ; leukocyte sticking ; oxygen radicals
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Although small intestine is frequently injured in endotoxin shock, the exact pathological sequence has not been fully understood. The major objective of this study is to elucidate the role of interleukin (IL)-1 in endotoxin-induced microcirculatory disturbance of rat small intestine. Mucosal and submucosal microvessels of the rat ileum were observed by intravital microscope with a high speed video camera system and the attenuating effect of E5090, an inhibitor of IL-1 generation, on endotoxin-induced intestinal microcirculatory disturbances was investigated. Endotoxin infusion produced significant mucosal damage, but before these morphological changes became significant, microvascular stasis in villi, decreased red blood cell velocity, and increased leukocyte adherence to venular walls were observed in intestinal microcirculatory beds 30 min after endotoxin administration. Intestinal IL-1α levels were also significantly increased at that time. Endotoxin treatment enhanced chemiluminescence activity from neurophils and rapidly mobilized CD18 on leukocytes. E5090, which suppressed the IL-1 production in intestinal mucosa, attenuated the microcirculatory disturbances induced by endotoxin, and significantly reduced the subsequent mucosal damage. E5090 also attenuated the increased chemiluminescence activity and CD18 expression on leukocytes. In conclusion, the production of IL-1α is enhanced in the intestinal mucosa during endotoxin infusion. IL-1 may be an important mediator of microcirculatory changes, including decreased red blood cell velocity and increased leukocyte sticking and its activation, leading to the mucosal damage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02100147
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  • 8
    Electronic Resource
    Electronic Resource
    Increased Nitric Oxide Production and Inducible Nitric Oxide Synthase Activity in Colonic Mucosa of Patients with Active Ulcerative Colitis and Crohn's Disease (1997)
    Springer
    Digestive diseases and sciences 42 (1997), S. 1047-1054 
    Details
    ISSN: 1573-2568
    Keywords: NITRIC OXIDE ; ULCERATIVE COLITIS ; CROHN'S DISEASE
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It is postulated that an enhanced production ofnitric oxide by inflamed intestine plays a role in thepathophysiology of active inflammatory bowel disease. Inthis study, systemic NOx concentrations and colonic nitric oxide synthase activity weredetermined in patients with ulcerative colitis orCrohn's disease. The relationship between these twoparameters and disease activity, as well as differences in nitric oxide synthase activity betweenulcerative colitis and Crohn's disease, were areas ofspecific focus. Patients with active ulcerative colitisand Crohn's disease had significantly elevated plasma NOx concentrations; a positivecorrelation was found between NOx values andinducible nitric oxide synthase activities in the activemucosa of these patients. In active ulcerative colitis,levels of inducible nitric oxide synthase were significantlyelevated in both normal and inflamed mucosa, althoughinducible nitric oxide synthase activity was higher inthe latter. These colonic inducible nitric oxidesynthase activities correlated well with the results ofendoscopic and histologic grading of inflammation. Therewas no increase in constitutive nitric oxide synthaseactivity in patients with active ulcerative colitis. However, constitutive nitric oxidesynthase activity was significantly increased in theinflamed mucosa in patients with Crohn's disease. InCrohn's disease, elevated inducible nitric oxidesynthase activity was found in both normal and inflamedmucosa, with no significant difference between thetissues. Such differences in nitric oxide production inthe colonic mucosa possibly reflect the significant differences in the pathophysiology andcharacteristic clinical features between ulcerativecolitis and Crohn's disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1018849405922
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  • 9
    Electronic Resource
    Electronic Resource
    Conjugated bile salts regulate turnover of rat intestinal brush border membrane hydrolases (1995)
    Springer
    Digestive diseases and sciences 40 (1995), S. 1193-1198 
    Details
    ISSN: 1573-2568
    Keywords: brush border membrane ; alkaline phosphatase ; bile salts ; pancreatic protease ; enzyme turnover ; biliary diversion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The mechanisms whereby the conjugated bile salts regulate the activities of the brush border membrane hydrolases and its physiological significance were investigated in rat small intestine, and comparisons were made with the action of pancreatic protease. Rat brush border membrane proteins were metabolically labeled with [35S]methionine, and isolated brush border membrane was incubated with taurocholate or pancreatic elastase. The activity of solubilized hydrolases was assayed and the molecular forms of the hydrolases were examined by SDS-PAGE. The activity and protein bands of alkaline phosphatase and sucrase-isomaltase were solubilized by taurocholate, while alkaline phosphatase was not solubilized by elastase. Solubilized sucrase-isomaltase molecules were proteolytically degraded by elastase, whereas the intact molecule of sucrase-isomaltase was solubilized by taurocholate. Next the physiological role of bile salts in brush border membrane hydrolase turnover were investigated using metabolic labeling of brush border membrane hydrolase and immunoprecipitation in biliary diversion rats. After three days of biliary diversion, a significant increase in alkaline phosphatase activity was observed. Although synthesis of alkaline phosphatase in biliary diversion rats was similar to that observed in control rats, biliary diversion rats showed 1.5-fold slower turnover of alkaline phosphatase when compared with control rats. These results suggest that conjugated bile salts in the intestinal lumen may cause a rapid turnover of brush border membrane hydrolases, which may be increased by the enhanced enzyme degradation. The mechanisms for the enhanced degradation appeared to be solubilization of hydrolases caused by the detergent activity of bile salts. Therefore, conjugated bile salts may play an important physiological role in the regulation of expression of the protease-resistant enzymes such as alkaline phosphatase.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02065523
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  • 10
    Electronic Resource
    Electronic Resource
    Tissue-type plasminogen activator of colonic mucosa in ulcerative colitis (1992)
    Springer
    Digestive diseases and sciences 37 (1992), S. 307-311 
    Details
    ISSN: 1573-2568
    Keywords: ulcerative colitis ; tissue-type plasminogen activator ; plasminogen activator inhibitor-1 ; endothelial cell ; fibrinolysis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Microvascular endothelial alterations are thought to be a crucial step for development of hemorrhagic changes in various pathological states. In this study, we determined the activity and amount of tissue-type plasminogen activator (t-PA) in the biopsy specimens from sigmoid colon of patients with ulcerative colitis to evaluate endothelial alterations and vascular changes of permeability. The results of this investigation revealed that mucosal amount of t-PA in the active stage of ulcerative colitis was two- to threefold higher than in healthy controls, while t-PA levels in plasma samples showed no remarkable differences among the groups. Increased t-PA activity appeared to correlate well to the degree of inflammation of colonic mucosa, and t-PA amount was still increased in the inactive stage. The present study indicates that t-PA determination in colonic biopsy specimens may be useful for the evaluation of clinical activity of ulcerative colitis in terms of the mucosal microvascular endothelial changes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01308189
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