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1

Neurally-mediated and neurally-independent beneficial actions of melatonin in the gastrointestinal tract

100%

Reiter R. J., Tan D-X., Mayo J. C., Sainz R. M., Leon J., Bandyopadhyay D.

Journal of Physiology and Pharmacology. Supplement

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2003

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tom 54

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nr 4

113-125

Melatonin (N-acetyl-5-methoxytryptamine), originally discovered in the pineal gland, is now known also to be present in the gastrointestinal tract from the stomach to the colon. It is localized and likely synthesized in the enterochromaffin cells of the mucosal lining. Its functions in the gut generally seem to be protective of the mucosa from erosion and ulcer formation and to possibly influence movement of the gastrointestinal contents through the digestive system. In this brief review, we summarize the work documenting the function of melatonin in influencing bicarbonate secretion in the stomach and its role in preventing and repairing ulcers in the stomach and duodenum. Melatonin’s actions in the control of bicarbonate secretion involve the central and peripheral sympathetic nervous systems and the actions are receptor mediated. Conversely, melatonin’s actions in reducing ulcer formation also seemingly involve the ability of the indole to directly scavenge toxic oxygen-based reactants, e.g., the hydroxyl radical, and possibly to promote antioxidative enzyme activities. These same processes may be involved in the mechanisms by which melatonin promotes ulcer healing. Additionally, however, melatonin’s effects on the healing of ulcers includes actions of blood flow in the margins of the ulcer and also on the sensory nerves. All indications are that melatonin has a variety of beneficial effects in the gastrointestinal tract. It is likely, however, that additional actions of melatonin on the digestive system will be uncovered.

2

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"Indolent ulcer" in Boxer

100%

Bryla P. K.

Okulistyka Weterynaryjna. e-kwartalnik dla lekarzy i studentów weterynarii

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2011

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nr 3

Artykuł przedstawia przypadek leczenia wrzodu rogówki u psa rasy bokser. Wrzód ten określany jest terminem "trudnogojący się" lub "indolent ulcer". Wrzody tego typu są predylekcyjne dla niektórych ras psów. Powstają często spontanicznie i niestety często mogą nawracać. istota choroby polega na oddzielaniu się nabłonka rogówki od jej istoty właściwej. Przyczyną tego może być wada hemidesmosomów, które odpowiadają za przyleganie nabłonka do stromy lub też procesy zwyrodnieniowe stromy rogówki. W obrazie klinicznym, po wybarwieniu rogówki za pomocą fluoresceiny, widoczne jest podciekanie barwnika pod warstwy rogówki. Istnieje kilka metod leczenia tego typu owrzodzenia. wymienić należy; keratotomię, powierzchowną keratektomię, chirurgiczne usunięcie martwego nabłonka rogówki. Leczeniu chirurgicznemu zawsze towarzyszy leczenie farmakologiczne. W naszym przypadku u psa zastosowaliśmy leczenie za pomocą keratotomii kratkowej skojarzonej z leczeniem farmakologicznym.

3

Involvement of heat shock proteins in the healing of acetic acid-induced gastric ulcers in rats

100%

Tsukimi Y., Nakai H., Itoh S., Amagase K., Okabe S.

Journal of Physiology and Pharmacology

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2001

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tom 52

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nr 3

4

Role of p38 mitogen-activated protein kinase in the healing of gastric ulcers in rats

100%

Kabayashi N., Kataoka T., Ono A., Tsukimi Y., Okabe S.

Journal of Physiology and Pharmacology

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2001

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tom 52

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nr 2

5

Dual action of nitric oxide in pathogenesis of indomethacin-induced small intestinal ulceration in rats

100%

Tanaka A., Kunikata T., Mizoguchi H., Kato S., Takeuchi K.

Journal of Physiology and Pharmacology

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1999

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tom 50

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nr 3

6

Characterization of 'unhealed gastric ulcers' produced with chronic exposure of acetic acid ulcers to indomethacin in rats

100%

Amagase K., Yokota M., Tsukimi Y., Okabe S.

Journal of Physiology and Pharmacology

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2003

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tom 54

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nr 3

We previously discovered that a 4-wk course of indomethacin delivered to rats with acetic acid ulcers resulted in production of "unhealed gastric ulcers" that persisted for up to 12 wks after treatment cessation. The present study examined the mechanism underlying such "unhealed gastric ulcers" with biochemical and histological procedures. "Unhealed gastric ulcers" were induced with a 4-wk indomethacin treatment (1 mg/kg, twice daily) in rats with acetic acid ulcers. Two and 4 wks after treatment cessation, ulcer size was significantly larger in rats receiving indomethacin compared with control animals. Ulcerated tissue prostaglandin E2 levels were significantly lower during indomethacin treatment, but the levels tended to increase after treatment cessation compared with levels measure in the group receiving vehicle. Myeloperoxidase activity levels were significantly higher during indomethacin treatment; such levels persisted after treatment cessation. Histologically, greater degrees of fibrosis and neutrophil accumulation, as well as a lesser degree of angiogenesis were observed in the "unhealed gastric ulcers" compared to ulcers that healed in a normal fashion. It was concluded that severe fibrosis, persistent neutrophil infiltration, and poor angiogenesis in the ulcer base might represent factors involved in the mechanism underlying production of "unhealed gastric ulcers".

7

Evidence for an infarctive pathogenesis of acute and chronic gastroduodenal ulceration

100%

Piasecki C.

Journal of Physiology and Pharmacology

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1992

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tom 43

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nr 2

It is clear that all mucosal defensive mechanisms acting against aggressive ulcerogenic factors depend on adequate blood flow. When defence is active, ulcers tend to heal and do so faster when luminal aggression is prevented by reduction of acidity or eradication of H. pylori. Such successful treatment is so profitable that pharmaceutical companies invest vast fortunes on research into every aspect of therapy. This may explain why research on basic aetiology has been slower. Nevertheless there have been recent advances which increasingly point towards an ischaemic pathogenesis of both acute and chronic ulcers. We have been studying those ischaemic mechanisms that may be triggered by alteration of normal physiological processes, and we now have a body of evidence supporting an infarction-like mechanism induced by abnormal motility which might explain the initiation of both acute and chronic human ulceration. In this article we review the evidence for this and show that such a pathogenesis is compatible with the features and current concepts of gastro-duodenal ulceration. Perhaps the most striking feature of chronic ulcers is their singularity, and localisation to the lesser curvature and first part of the duodenum. Within the lesser curvature there is an increasing incidence from the oesophageal end towards pylorus, with maximal incidence in the incisural area (1). Duodenal ulcers occur on the anterior or posterior walls of the first 4 cm. uncommonly on the superior “cap” and rarely on the inferior wall. Such localisation points to a primary cause which, by analogy with other localised necroses eg coronary or stroke, is usually an infarction of an end-artery system.

8

Serological differentiation of Helicobacter pylori CagA[plus] and CagA[minus] infections

100%

Chmiela M., Wisniewska M., Bak-Romaniszyn L., Rechcinski T., Planeta-Malecka I., Bielanski W., Konturek S. J., Plonka M., Klink M., Rudnicka W.

Archivum Immunologiae et Therapiae Experimentalis

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2003

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tom 51

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nr 2

9

Association of the presence the Helicobacter pylori in the oral cavity and in the stomach

80%

Czesnikiewicz-Guzik M., Karczewska E., Bielanski W., Guzik T. J., Kapera P., Targosz A., Konturek S. J., Loster B.

Journal of Physiology and Pharmacology. Supplement

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2004

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tom 55

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nr 2

105-115

Helicobacter pylori is a gram-negative, microaerophilic rod-shaped bacteria that lives beneath the gastric mucous layer, on the surface of epithelial cells. Stomach infection with this organism causes inflammation of the gastric mucosa, which can lead to gastritis, duodenal or gastric ulcer and even in rare cases to gastric carcinoma or MALT lymphoma. Approximately 50% of the world's population is believed to be infected with H. pylori. Most infections is probably acquired in childhood, but the exact route of transmission is unknown. It has been speculated that dental plaque might harbour Helicobacter pylori and, therefore, might be a source of gastric infection. In order to address this issue we studied the relationships between oral and gastric infections with H. pylori in 100 subjects. Methods: Gastric H. pylori infection was determined by 13C-urea breath test (UBT) and the presence of the bacteria in oral cavity was monitored by the culture from the saliva and from dental plaque. Results: H. pylori was found in the stomach in 51% of studied individuals, while oral H. pylori was found in 54% (in saliva) and in 48.3% (in gingival pockets), the difference was not statistical significant (p=NS). Interestingly, anti-Hp IgA was found in 84% of studied individuals. No relationship was found between the presence of the bacteria in the oral cavity and the H. pylori gastric infection. 54.9% of subjects with stomach infection showed concomitant presence of H. pylori in saliva. 53.2% of examined subjects with negative UBT-test revealed the presence of H. pylori in culture from the saliva. The X2 value of relationship between UBT and culture H pylori in saliva was 0.029 (p=0.9). Similarly, no relationship was found between the presence of H. pylori in the stomach and in the dental plaque (X2=0.6; p=0.4). As expected, the presence of H. pylori in the dental plaque was significantly correlated with the presence of bacteria in the saliva (X2=18.4; p=0.0002). We also compared the presence of H. pylori in the saliva of patients with and without teeth. The cultured H. pylori was found in 63.7% of patients without teeth and in 52.9% of patients with teeth. This indicates that the presence of teeth does not seem to affect the occurrence of H. pylori in saliva. We conclude that oral cavity contamination with of H. pylori occurs at similar degree to that in the stomach. However, there was no significant correlation between the occurrence of H. pylori in the stomach and in the oral cavity indicating that other factors, like susceptibility to infection due to acid environment in the stomach may be the major factor in gastric infection with that bacteria, while oral cavity may serve only as transient food-related contamination without clear relation to gastric infection.

10

Antral ulcers induced by alendronate, a nitrogen-containing bisphosphonate, in rat stomachs - prophylactic effect of rebamipide

80%

Ohashi Y., Aihara E., Takasuka H., Takahashi K., Takeuchi K.

Journal of Physiology and Pharmacology

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2009

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tom 60

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nr 3

85-93

We demonstrated the development of antral ulcers induced in rats by alendronate and investigated the pathogenic factors involved in this model. Animals fasted for 18 h were given alendronate p.o., and then re-fed normally and killed on various days up to 7 days later. Alendronate caused non-hemorrhagic damage in both the corpus and antrum of fasted rats, but after refeeding for 3 days the lesions in the corpus healed completely, while those in the antrum developed into large ulcers with increased vascular permeability. The development of antral ulcers was accompanied by an increase in MPO activity and lipid peroxidation as well as a decrease in SOD activity and GSH content in the mucosa. Histologically, the damage did not penetrate the muscularis mucosa, yet severe edema and neutrophil infiltration were observed in the submucosa. Neither omeprazole nor indomethacin had any effect, while allopurinol and SOD reduced the severity of these ulcers. Rebamipide dose-dependently suppressed the ulcerogenic response to alendronate, with a concomitant reversal of the increased vascular permeability, MPO activity and lipid peroxidation as well as the reduced SOD activity and GSH content. These results suggest that alendronate did not cause gross damage in the stomach of fasted rats, yet produced large ulcers in the antrum with severe edema after refeeding. The pathogenesis of these ulcers may be explained by impairment of the mucosal anti-oxidative system and does not involve acid/peptic digestion and deficiency of prostaglandins. Rebamipide prevents the antral ulcers, probably due to its anti-oxidative as well as anti-inflammatory actions.

11

Aspirin’s ability to induce intestinal injury in rats is dependent on bile and can be reversed if pre-associated with phosphatidylcholine

80%

Lichtenberger L. M., Phan T., Okabe S.

Journal of Physiology and Pharmacology

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2011

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tom 62

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nr 4

12

Gastroprotection by pentoxyfilline against stress-induced gastric damage. Role of lipid peroxidation, antioxidizing enzymes and proinflammatory cytokines

80%

Kwiecien S., Brzozowski T., Konturek P. C., Pawlik M. W., Pawlik W. W., Kwiecien N., Konturek S. J.

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 2

Impairment of blood perfusion in gastric mucosa results in the formation of erosions and ulcers. Nitric oxide (NO), produced via activity of NO-synthase (NOS), appears to be a one of major factors, involved in the regulation of the gastric blood flow (GBF). Inhibition of this enzyme by N-nitro-L-arginine (L-NNA) results in local decrease of NO production, reduces GBF and impairs gastric mucosal integrity, the effects that can be reversed by the pretreatment with L-arginine, the NOS substrate. However, little information is available regarding the contribution of reactive oxygen species (ROS)-induced lipid peroxidation and NO to the mechanism of gastric mucosal integrity. Therefore, the aim of our present study was to determine the action of pentoxyfilline (PTX), an inhibitor of tumor necrosis factor alpha (TNFalpha) with or without NOS inhibition by L-NNA administration in rats with water immersion and restraint stress (WRS)-induced gastric lesions . Experiments were carried out on 100 male Wistar rats. The gastric blood flow (GBF) was measured using laser Doppler flowmeter. The area of gastric lesions was determined by planimetry and the levels of proinflammatory cytokines (IL-1ß and TNFalpha) were measured by ELISA. Colorimetric assays were employed to determine gastric mucosal levels of lipid peroxidation products, such as malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) and antioxidant enzymes including superoxide dismutase (SOD) activity, as well as tissue concentration of reduced glutathione (GSH). Administration of PTX significantly attenuated the gastric lesions, induced by 3.5 h of WRS and this was accompanied by the rise in the GBF and a significant decrease in plasma proinflammatory cytokines (IL-1ß and TNFalpha) levels, as well as the reduction of lipid peroxidation. Exposure of rats to WRS supressed the SOD and GSH activities and these effects were reversed by PTX. The protective and hyperemic effects of PTX, as well as an increase in mucosal SOD activity and GSH concentration were counteracted by pretreatment with L-NNA, but restored by the pretreatment with L-arginine, a NOS substrate. We conclude that PTX exerts beneficial, gastroprotective effect against WRS-induced gastric lesions due to enhancement in gastric microcirculation, possibly mediated by the enhanced NOS activity as well as local action of NO and by the attenuation of oxidative metabolism and generation proinflammatory cytokines.

13

Cyclooxygenase-2 selective and nitric oxide-releasing nonsteroidal anti-inflammatory drugs and gastric mucosal responses

80%

Takeuchi K., Suzuki K., Yamamoto H., Araki H., Mozoguchi H., Ukawa H.

Journal of Physiology and Pharmacology

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1998

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tom 49

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nr 4

14

Prevention and treatment of ulcers induced by nonsteroidal anti-inflammatory drugs: an update

80%

Dajani E. Z., Agrawal N. M.

Journal of Physiology and Pharmacology

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1995

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tom 46

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nr 1

15

Novel environment as a stress-inducing factor. An event-related potentials study

80%

Michalski A.

Acta Neurobiologiae Experimentalis

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1998

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tom 58

|

nr 3

16

Role of basic fibroblast growth factor in the suppression of apoptotic caspace-3 during chronic gastric ulcer healing

80%

Slomiany B. L., Piotrowski J., Slomiany A.

Journal of Physiology and Pharmacology

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1998

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tom 49

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nr 4

17

Stomach wall changes caused by the presence of third-stage Anisakis simplex B larvae in infected dogs

80%

Podolska M., Piusinski W., Rokicki J.

Acta Parasitologica

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1997

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tom 42

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nr 4

Samples of stomach fundus and pylorus tissue collected from eight dogs experimentally infected with third-stage A. simplex В larvae were examined macro- and microscopically. The histopathological changes in these samples were analysed. Pathomorphological examination revealed that A. simplex В larvae actively penetrated the dog’s stomach wall within 2 days of infection. The presence of larvae in the mucous membrane was accompanied by tissue damage and cell infiltration predominantly by eosinophils.

18

Mechanism by which indomethacin delays the healing of acetic acid-induced ulcers in rats. Role of neutrophil antichemotactic and chemotactic activities

80%

Fujita H., Takahashi S., Okabe S.

Journal of Physiology and Pharmacology

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1998

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tom 49

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nr 1

19

13C-urea breath test for detection of Helicobacter pylori and its correlation with endoscopic and histologic findings

80%

Hilker E., Domschke W., Stoll R.

Journal of Physiology and Pharmacology

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1996

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tom 47

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nr 1

20

A new ulcer model unhealed gastric ulcers, induced by chronic treatment with indomethacin in rats with acetic acid ulcers

80%

Amagase K., Okabe S.

Journal of Physiology and Pharmacology

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1999

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tom 50

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nr 2

Ograniczanie wyników

Neurally-mediated and neurally-independent beneficial actions of melatonin in the gastrointestinal tract

"Indolent ulcer" in Boxer

Involvement of heat shock proteins in the healing of acetic acid-induced gastric ulcers in rats

Role of p38 mitogen-activated protein kinase in the healing of gastric ulcers in rats

Dual action of nitric oxide in pathogenesis of indomethacin-induced small intestinal ulceration in rats

Characterization of 'unhealed gastric ulcers' produced with chronic exposure of acetic acid ulcers to indomethacin in rats

Evidence for an infarctive pathogenesis of acute and chronic gastroduodenal ulceration

Serological differentiation of Helicobacter pylori CagA[plus] and CagA[minus] infections

Association of the presence the Helicobacter pylori in the oral cavity and in the stomach

Antral ulcers induced by alendronate, a nitrogen-containing bisphosphonate, in rat stomachs - prophylactic effect of rebamipide

Aspirin’s ability to induce intestinal injury in rats is dependent on bile and can be reversed if pre-associated with phosphatidylcholine

Gastroprotection by pentoxyfilline against stress-induced gastric damage. Role of lipid peroxidation, antioxidizing enzymes and proinflammatory cytokines

Cyclooxygenase-2 selective and nitric oxide-releasing nonsteroidal anti-inflammatory drugs and gastric mucosal responses

Prevention and treatment of ulcers induced by nonsteroidal anti-inflammatory drugs: an update

Novel environment as a stress-inducing factor. An event-related potentials study

Role of basic fibroblast growth factor in the suppression of apoptotic caspace-3 during chronic gastric ulcer healing

Stomach wall changes caused by the presence of third-stage Anisakis simplex B larvae in infected dogs

Mechanism by which indomethacin delays the healing of acetic acid-induced ulcers in rats. Role of neutrophil antichemotactic and chemotactic activities

13C-urea breath test for detection of Helicobacter pylori and its correlation with endoscopic and histologic findings

A new ulcer model unhealed gastric ulcers, induced by chronic treatment with indomethacin in rats with acetic acid ulcers