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Urea-urease system in cytoprotection against acute mucosal damage

100%

Brzozowski T., Sliwowski Z., Majka J., Drozdowicz D., Konturek S. J.

Journal of Physiology and Pharmacology

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1996

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tom 47

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nr 1

2

Leptin, gastrointestinal and stress hormones in response to exercise in fasted or fed subjects and before or after blood donation

100%

Sliwowski Z., Lorens K., Konturek S. J., Bielanski W., Zoladz J. A.

Journal of Physiology and Pharmacology

|

2001

|

tom 52

|

nr 1

3

Involvement of sensory afferent fibers and lipid peroxidation in the pathogenesis of stress-induced gastric mucosa damage

86%

Kwiecien S., Pawlik M. W., Sliwowski Z., Kwiecien N., Brzozowski T., Pawlik W. W., Konturek S. J.

Journal of Physiology and Pharmacology. Supplement

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2007

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tom 58

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nr 3

149-162

4

Probiotic bacteria Escherichia coli strain Nissle 1917 attenuates acute gastric lesions induced by stress

86%

Konturek P. C., Sliwowski Z., Koziel J., Ptak-Belowska A., Burnat G., Brzozowski T., Konturek S. J.

Journal of Physiology and Pharmacology. Supplement

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2009

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tom 60

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nr 6

5

Application of a diagnostic-therapeutic procedure using implant-supported dental prosthesis as a preventive therapy for candidiasis of upper gastrointestinal tract in complete denture users

86%

Majewski S., Loster B. W., Macura A. B., Wisniewska G., Sliwowski Z., Mazurkiewicz-Janik M., Konturek S. J.

Journal of Physiology and Pharmacology. Supplement

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2008

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tom 59

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nr 5

39-46

6

Duodenal mucosal protection by bicarbonate secretion and its mechanisms

86%

Konturek S. J., Konturek P. C., Pawlik T., Sliwowski Z., Ochmanski W., Hahn E. G.

Journal of Physiology and Pharmacology. Supplement

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2004

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tom 55

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nr 2

5-17

Proximal portion of duodenum is exposed to intermittent pulses of gastric H+ discharged by the stomach. This review summarizes the mechanisms of duodenal mucosal integrity, mainly the role of mucus-alkaline secretion and the mucous barrier protecting surface epithelium against gastric H+. The mucous barrier protects the leaky duodenal epithelium against each pulse of gastric H+, which penetrates this barrier and diffuses into duodenocytes, but fails to damage them due to; a) an enhanced expression of cyclooxygenase-1 (COX-1), with release of protective prostaglandins (PG) and of nitric oxide (NO) synthase (NOS) with, however, production of NO, stimulating duodenal HCO3- secretion and b) the release of several neurotransmitters also stimulating HCO3- secretion such as vasoactive intestimal peptide (VIP), pituitary adenylate-cyclase activating polypeptide (PACAP), acetylcholine, melatonin, leptin and ghrelin released by enteric nerves and mucosal cells. At the apical duodenocyte membrane at least two HCO3-/Cl- anion exchangers operate in response to luminal H+ to provide adequate extrusion of HCO3- into duodenal lumen. In the basolateral portion of duodenocyte membrane, both non-electrogenic (NBC) and electrogenic (NBCn) Na+-HCO3- cotransporters are activated by the exposure to duodenal acidification, causing inward movement of HCO3- from extracellular fluid to duodenocytes. There are also at least three Na+/H+ (NHE1-3) amiloride-sensitive exchangers, eliminating H+ which diffused into these cells. The Helicobacter pylori (Hp) infection and gastric metaplasia in the duodenum with bacterium inoculating metaplastic mucosa and inhibiting HCO3- secretion by its endogenous inhibitor, asymetric dimethyl arginine (ADMA), may result in duodenal ulcerogenesis.

7

Effect of different muscle shortening velocities during prolonged incremental cycling exercise on the plasma growth hormone, insulin, glucose, glucagon, cortisol, leptin and lactate concentrations

86%

Zoladz J. A., Duda K., Konturek S. J., Sliwowski Z., Pawlik T., Majerczak J.

Journal of Physiology and Pharmacology

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2002

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tom 53

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nr 3

Strenuous exercise was reported to involve the alteration in the release of some "stress" hormones such as growth hormone (GH), cortisol, catecholamines and appropriate adjustment of energy metabolism but the relative contribution of these hormones to metabolic response, to cycling exercise performed at different muscle shortening velocities, has not been clarified. Aims: The purpose of this experiment was to assess the effect of applying different pedalling rates during a prolonged incremental cycling exercise test on the changes in the plasma levels of growth hormone, cortisol, insulin, glucagon and leptin in humans. Material and Methods: Fifteen healthy non-smoking men (means ± SD: age 22.9 ± 2.4 years; body mass 71.9 ± 8.2 kg; height 178 ± 6 cm; with VO2max of 3.896 ± 0.544 l . min-1), assessed in laboratory tests, were subjects in this study. The subjects performed in two different days a prolonged incremental exercise tests at two different pedalling rates, one of them at 60 and another at 120 rev . min-1. During this tests the power output has increased by 30 W every 6 minutes. The tests were stopped when the subject reached about 70 % of the VO2max. Results and conclusions: We have found that choosing slow or fast pedalling rates (60 or 120 rev . min-1), while generating the same external mechanical power output, had no effect on the pattern of changes in plasma cortisol, insulin, glucagon, glucose and leptin concentrations. But, generation of the same external mechanical power output at 120 rev . min-1 causes more stepper increase (p < 0.01) in the plasma growth hormone concentration [GH]pl and plasma lactate concentrations [La]pl when compared to that observed during cycling at 60 rev . min-1. We have also found that the onset of a significant increase in [GH]pl during cycling at 60 rev . min-1 was not accompanied by significant increase in [La]pl. While during cycling at 120 rev . min-1 the onset of a significant increase in [La]pl occurred without increase in [GH]pl, but with continuation of exercise when plasma [La]pl increased, there was also a parallel rise in plasma [GH]pl, as reported before. This results indicates that the increase in [GH]pl during exercise is not closely related to the increase in [La]pl.

8

Effect of moderate incremental exercise, performed in fed and fasted state on cardio-respiratory variables and leptin and ghrelin concentrations in young healthy men

86%

Zoladz J. A., Konturek S. J., Duda K., Majerczak J., Sliwowski Z., Grandys M., Bielanski W.

Journal of Physiology and Pharmacology

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2005

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tom 56

|

nr 1

Background: Although hormonal responses to exercise performed in fed state are well documented, far less in known about the effect of a single exercise bout, performed after overnight fasting, on cardio-respiratory responses and hormones secretion. It has been reported that recently discovered hormones as leptin and ghrelin may affect cardiovascular responses at rest. However, their effect on the cardiovascular responses to exercise is unknown. Aims: This study was designed to determine the effect of overnight fasting on cardio- respiratory responses during moderate incremental exercise. We have hypothesised that fasting / exercise induced changes in plasma leptin / ghrelin concentrations may influence cardiovascular response. Material and Methods: Eight healthy non-smoking men (means ± SE.: age 23.0 ± 0.5 years; body mass 71.9 ± 1.5 kg; height 179.1 ± 0.8 cm; BMI 22.42 ± 0.49 kg . m-2 with VO2max of 3.71 ± 0.10 l . min-1) volunteered for this study. The subjects performed twice an incremental exercise test, with the increase of power output by 30 W every 3 minutes. Tests were performed in a random order: once in the feed state - cycling until exhaustion and second, about one week later, after overnight fasting - cycling until reaching 150 W. Results: In the present study we have compared the results obtained during incremental exercise performed only up to 150 W (59 ± 2 % of VO2max) both in fed and fasted state. Heart rate measured during exercise at each power output, performed in fasted state was by about 10 bt . min-1 (p = 0.02) lower then in fed subjects. Respiratory quotient and plasma lactate concentration in fasted state were also significantly (p<0.001) lower than in the fed state. Pre-exercise plasma leptin and ghrelin concentrations were not significantly different in fed and fasted state. Exercise induced increase in hGH was not accompanied by a significant changes in the studied gut hormones such as ghrelin, leptin, and insulin, except for plasma gastrin concentration, which was significantly (p = 0.008) lower in fasting subjects at the power output of 150 W. Plasma [IL-6] at rest before exercise performed in fasted state was significantly (p = 0.03) elevated in relation to the fed state. This was accompanied by significantly higher (p = 0.047) plasma noradrenaline concentration. Plasma IL-6 concentration at rest in fed subjects was negatively correlated with plasma ghrelin concentration (r = - 0.73, p < 0.05) and positively correlated with plasma insulin concentration (r = 0.78, p < 0.05). Significant negative correlation (r = - 0.90; p < 0.05) was found between plasma insulin and ghrelin concentration at rest in fed subjects. Conclusions: We have concluded that plasma leptin and ghrelin concentrations have no significant effect on the fasting-induced attenuation of heart rate during exercise. We have postulated that this effect is caused by increased plasma norepinephrine concentration, leading to the increase in systemic vascular resistance and baroreceptor mediated vagal stimulation. Moreover we believe, that the fasting-induced significant increase in plasma IL-6 concentration at rest, accompanied by higher plasma norepinephrine concentration and lower RQ, belongs to the physiological responses, maintaining energy homeostasis in the fasting state.

9

SU-840, a novel synthetic flavonoid derivative of sophoradin, with potent gastroprotective and ulcer healing activity

86%

Brzozowski T., Konturek S. J., Kwiecien S., Pajdo R., Drozdowicz D., Sliwowski Z., Muramatsu M.

Journal of Physiology and Pharmacology

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1998

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tom 49

|

nr 1

10

Effects of biofeedback training on esophageal peristaltis in amyotrophic lateral sclerosis [ALS] patients with dysphagia

86%

Lorens K., Tomik B., Pichor A., Szczudlik A., Sliwowski Z., Konturek S. J.

Journal of Physiology and Pharmacology. Supplement

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2001

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tom 52

|

nr 2

11

Adaptive cytoprotection by ammonia and urea - urease system in the rat gastric mucosa

86%

Brzozowski T., Konturek P., Sliwowski Z., Szlachcic A., Hahn E. G., Konturek S. J.

Journal of Physiology and Pharmacology

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1995

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tom 46

|

nr 4

12

Nitric oxide (NO)-releasing aspirin and (NO) donors in protection of gastric mucosa against stress

86%

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

Journal of Physiology and Pharmacology. Supplement

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2008

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tom 59

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nr 2

Acute gastric mucosal lesions represent an important clinical problem. The experimental model of acute gastritis such as water immersion restraint (WRS) stress is useful tool in examination of pathomechanism of acute gastric damage. Nitric oxide (NO) plays an important role in the maintenance of gastric barrier, however the role of reactive oxygen species (ROS) in the interaction between NO and gastric mucosa integrity has been little studied. The purpose of our present study was to explain the participation of ROS in healing of WRS-induced gastric lesions accelerated by NO. Experiments were carrying out on 120 male Wistar rats. To assess gastric blood flow (GBF) laser Doppler flowmeter was used. The number of gastric lesions was established by planimetry. The colorimetric assays were used to determine gastric tissue level of malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE), the products of lipid peroxidation by ROS, as well as superoxide dismutase (SOD) activity, the enzyme scavanger of ROS. We demonstrated that 3.5 h of WRS resulted in appearance of acute gastric mucosal lesions accompanied by a significant decrease of GBF. Biological effects of ROS were estimated by measuring tissue level of MDA and 4-HNE, as well as the SOD activity. It was demonstrated that 3.5 h of WRS led to significant increase of MDA and 4-HNE mucosal level, that was accompanied by a decrease of SOD activity. Pretreatment with NO-donors (SIN-1, SNAP, nitroglycerin, NO-ASA) resulted in reduction of gastric lesions number, increment of GBF, decrease of MDA and 4-HNE tissue level and increase of SOD activity. Suppression of ROS play an important role in NO-donors action in gastroprotection against gastric acute lesions induced by 3.5 h of WRS. NO-donors cause an attenuation of lipid peroxidation as documented by a decrease of MDA and 4-HNE levels and enhancement of antioxidative properties as evidenced by increase of SOD activity.

13

Neural aspects of ghrelin-induced gastroprotection against mucosal injury induced by noxious agents

73%

Brzozowski T., Konturek P. C., Sliwowski Z., Drozdowicz D., Kwiecien S., Pawlik M., Pajdo R., Konturek S. J., Pawlik W. W., Hahn E. G.

Journal of Physiology and Pharmacology. Supplement

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2006

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tom 57

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nr 6

63-76

Ghrelin, identified in oxyntic mucosa has been recently implicated in the control of food intake and growth hormone (GH) release but whether this hormone can influence the gastric secretion and gastric mucosal integrity have been little studied. We compared the effects of intraperitoneal (i.p.) and intracerebroventricular (i.c.v.) administration of ghrelin on gastric secretion in rats equipped with gastric fistula (GF) and gastric lesions induced in rats by 75% ethanol and ischemia-reperfusion (I/R) with or without vagotomy or functional ablation of afferent sensory nerves by capsaicin. The number and the area of gastric lesions was measured by planimetry, the GBF was assessed by H2-gas clearance method and blood was withdrawn for the determination of the plasma ghrelin and gastrin levels. Ghrelin (5-80 µg/kg i.p. or 600-5000 ng/rat i.c.v.) increased gastric acid secretion and attenuated gastric lesions induced by ethanol and I/R. These protective effects of ghrelin were accompanied by the significant rise in the gastric mucosal blood flow (GBF) and plasma ghrelin and gastrin levels. Ghrelin given i.p. or injected i.c.v. in standard doses 20 µg/kg or 5000 ng/kg, respectively, significantly attenuated the gastric mucosal damage and significantly raised the GBF. Ethanol applied i.g. in smaller concentrations (12.5% and 25%) produced a significant increase in plasma immunorective ghrelin levels and this effect was inhibited in rats receiving ethanol in higher concentrations (75% and 100%). Ghrelin-induced protection after its i.p. or i.c.v. administration and accompanying increase in the GBF were completely abolished by vagotomy and capsaicin-deactivation of sensory nerves. Concurrent treatment with CGRP added to ghrelin restored the gastroprotective and hyperemic effects of ghrelin applied i.p. or i.c.v. in rats with capsaicin denervation. We conclude that central and peripheral ghrelin exerts a potent protective and gastric secretory effects in rats exposed to ethanol and I/R, and that these actions involve vagal nerve integrity, partially depending upon afferent nerves and hyperemia mediated by sensory neuropeptides such as CGRP released from these nerves.

14

Importance of luminal and mucosal zinc in the mechanism of experimental gastric ulcer healing

73%

Opoka W., Adamek D., Plonka M., Reczynski W., Bas B., Drozdowicz D., Jagielski P., Sliwowski Z., Adamski P., Brzozowski T.

Journal of Physiology and Pharmacology

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2010

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tom 61

|

nr 5

15

Interaction between selective cyclooxygenase inhibitors and capsaicin-sensitive afferent sensory nerves in pathogenesis of stress-induced gastric lesions. Role of oxidative stress

73%

Kwiecien S., Konturek P. C., Sliwowski Z., Mitis-Musiol M., Pawlik M. W., Brzozowski B., Jasnos K., Magierowski M., Konturek S. J., Brzozowski T.

Journal of Physiology and Pharmacology

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2012

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tom 63

|

nr 2

16

Nitric oxide (NO)-releasing aspirin exhibits a potent esophagoprotection in experimental model of acute reflux esophagitis. Role of nitric oxide and proinflammatory cytokines

73%

Pawlik M., Pajdo R., Kwiecien S., Ptak-Belowska A., Sliwowski Z., Mazurkiewicz-Janik M., Konturek S. J., Pawlik W. W., Brzozowski T.

Journal of Physiology and Pharmacology

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2011

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tom 62

|

nr 1

The purpose of this study was to develop an acute animal model of reflux esophagitis, which would be suitable to induce the esophageal damage caused by gastric acid reflux, thus mimicking the esophageal injury of human gastroesophageal reflux disease (GERD). Global research indicates that GERD is rapidly increasing among the world's population. NSAIDs are known to induce gastrointestinal damage and low doses of aspirin (ASA) have been shown to increase the incidences of GERD in humans. Gastric acid and pepsin secretion and enhanced COX-2 expression were implicated in the pathogenesis of reflux esophagitis, but the effect of selective COX-2 inhibitors against lesions induced by the reflux of gastric acid content into esophagus has not been thoroughly studied. Here, we compared the effect of aspirin (ASA) and so called "safe" nitric oxide (NO) derivative of ASA with those of non-selective and selective cyclooxygenase (COX)-1 and COX-2 in rat model of reflux esophagitis. Reflux esophagitis was induced in anesthetized rats by ligating the pylorus and limiting ridge transitional region between the forestomach and the corpus of stomach. Subsequently, the total gastric reservoir to store gastric juice was greatly diminished, resulting in the reflux of this juice into the esophagus. Rats with esophagitis received intragastric (i.g.) pretreatment either with: 1) vehicle (saline), 2) ASA or NO-ASA (100 mg/kg); 3) the non-selective COX inhibitor, indomethacin (5 mg/kg); 4) the selective COX-1 inhibitor, SC-560 (10 mg/kg), and 5) the selective COX-2 inhibitor, celecoxib (5 mg/kg). In a separate series of rats with reflux oesophagitis, the efficacy of ASA combined with a donor of NO, glyceryl trinitrate (GTN; 10 mg/kg i.g.) to prevent esophageal mucosal injury was investigated. Four hours after induction of esophagitis the gross mucosal damage was graded with a macroscopic lesion index (LI) from 0-6. The esophageal blood flow (EBF) was determined by H2-gas clearance technique, the oesophageal mucosal and blood samples were collected for histology and analysis of the RT-PCR expression and release of proinflammatory cytokines IL-1ß, TNF- and IL-6 using specific ELISA. The exposure of the esophagus to reflux of gastric acid time-dependently increased the esophageal LI and morphologic damage, and decreased EBF with the most significant changes observed at 4 hrs after the ligation procedure. The pretreatment with native ASA in the dose that suppressed the generation of mucosal PGE2, enhanced gross and histologic esophageal damage and produced a significant fall in EBF. NO-ASA or ASA coupled with GTN counteracted the aggravation of the damage and accompanying fall in EBF when compared with native ASA applied alone to rats with esophagitis. The proinflammatory cytokines IL-1ß and TNF- were overexpressed in rats with esophagitis and those pretreated with ASA but this effect was significantly attenuated by NO-ASA. Plasma IL-1ß, TNF- and IL-6 were negligible in the intact rats but significantly increased in those with esophagitis, with this effect being further enhanced by non-selective (indomethacin) and selective (SC-560, celecoxib) COX-1 and COX-2 inhibitors. We conclude that conventional NSAID such as aspirin augments esophagitis, while NO-ASA exerts the beneficial protective effect against reflux esophagitis via the enhancement of esophageal microcirculation due to NO release and an inhibitory effect on expression and release of pro-inflammatory cytokines.

17

Lipid peroxidation, reactive oxygen species and antioxidative factors in the pathogenesis of gastric mucosal lesions and mechanism of protection against oxidative stress - induced gastric injury

73%

Kwiecien S., Jasnos K., Magierowski M., Sliwowski Z., Pajdo R., Brzozowski B., Mach T., Wojcik D., Brzozowski T.

Journal of Physiology and Pharmacology

|

2014

|

tom 65

|

nr 5

18

Interaction of nonsteroidal anti-inflammatory drugs (NSAID) with Helicobacter pylori in the stomach of humans and experimental animals

73%

Brzozowski T., Konturek P. C., Sliwowski Z., Kwiecien S., Drozdowicz D., Pawlik M., Mach K., Konturek S. J., Pawlik W. W.

Journal of Physiology and Pharmacology. Supplement

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2006

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tom 57

|

nr 3

67-79

Helicobacter pylori (H. pylori) and non-steroidal anti-inflammatory drugs (NSAID) are major pathogenic factors in peptic ulcer disease but whether these two factors exert synergistic or antagonistic action on the gastric mucosa has been a subject of controversy. The classic concept states that there is an increased ulcer occurrence and bleeding in patients with both H. pylori infection and NSAID use. However, the question whether the H. pylori eradication therapy in NSAID users reduces the occurrence of peptic ulcer has not been fully addressed. Studies on secondary prevention of NSAID-associated ulcers in H. pylori patients have indicated that H. pylori eradication results in impaired ulcer healing with an effect on the rate of peptic ulcer occurrence. On the other hand, the treatment of H. pylori in patients with no prior history of chronic NSAID therapy has been shown to decrease the risk of peptic ulcer. Studies in experimental animals revealed for instance, that the H. pylori infection augments the gastric mucosal damage induced by NSAID in Mongolian gerbils. In rats with preexisting chromic gastric ulcers, H. pylori infection attenuated significantly the aspirin-induced inhibition of ulcer healing and accompanying fall in the gastric blood flow at the margin of these ulcers, suggesting negative interaction between aspirin and H. pylori on ulcerogenesis. Accumulated evidence in humans and animals shows that both aspirin and H. pylori upregulate the expression of cyclooxygenase (COX)-2 both at mRNA and protein levels at the ulcer margin, but failed to influence significantly that of COX-1. It was, therefore, proposed that H. pylori may in fact, antagonize, aspirin-induced delay of ulcer healing due to suppression of acid secretion by the enhancement in PGE2 possibly derived from COX-2 expression and activity and to the overexpression of growth factors such as TGFalpha and VEGF. The present review summarizes and further addresses the issue of the interaction between these two major ulcer risk factors determined in the stomach of humans and experimental animals.

19

Role of sensory afferent nerves, lipid peroxidation and antioxidative enzymes in the carbon monoxide-induced gastroprotection against stress ulcerogensis

73%

Kwiecien S., Magierowska K., Magierowski M., Surmiak M., Hubalewska-Mazgaj M., Pajdo R., Sliwowski Z., Chmura A., Wojcik D., Brzozowski T.

Journal of Physiology and Pharmacology

|

2016

|

tom 67

|

nr 5

20

Protective influence of melatonin against acute esophageal lesions involves prostaglandins, nitric oxide and sensory nerves

73%

Konturek S. J., Zayachkivska O., Havryluk X. O., Brzozowski T., Sliwowski Z., Pawlik M., Konturek P. C., Czesnikiewicz-Guzik M., Gzhegotsky M. R., Pawlik W. W.

Journal of Physiology and Pharmacology

|

2007

|

tom 58

|

nr 2

Melatonin (MT) is known to protect gastrointestinal mucosa against various types of injury but its effects on esophageal damage have not been studied. We examined the effects of MT on acute esophageal injury and the mechanism involved in the action of this indole. Acute esophageal lesions were induced by perfusion with acid-pepsin solution using tube inserted through the oral cavity into the mid of esophagus of anaesthetized rats with or without inhibition of prostaglandin (PG) generation by indomethacin (5 mg/kg/day), nitric oxide (NO) formation by NG-nitro-L-arginine (L-NNA, 20 mg/kg/day) or sensory nerves deactivation by capsaicin (125 mg/kg, sc). The esophageal injury was assessed by macroscopic score and histologic activity index. The esophageal mucosal blood flow (EBF) was determinated by H2-gas clearance method. The plasma TNF-alpha and nitrate/nitrite (NOx) levels and mucosal PGE2 contents were assessed by immunoassays. Esophageal acid-pepsin perfusion induced noticeable esophageal mucosal injury as compared to perfusion with vehicle saline. The pretreatment with MT prevented significantly esophageal injury, raised EBF and mucosal content of PGE2, while decreasing the levels of TNF-alpha. Inhibition of COX/PG and NOS/NO systems by indomethacin and L-NNA, respectively, or inactivation of sensory nerves by capsaicin, that manifested in further increase of esophageal injury, reduced the levels of EBF, markedly raised the levels TNF-alpha and reduced mucosal PGE2, but the pretreatment with MT prevented significantly esophageal injury, improved EBF and raised mucosal PGE2 contents. These studies suggest that MT can be considered as a novel esophagoprotector, acting, at least in part, through the COX/PG and NOS/NO systems and activation of sensory nerves.

Ograniczanie wyników

Urea-urease system in cytoprotection against acute mucosal damage

Leptin, gastrointestinal and stress hormones in response to exercise in fasted or fed subjects and before or after blood donation

Involvement of sensory afferent fibers and lipid peroxidation in the pathogenesis of stress-induced gastric mucosa damage

Probiotic bacteria Escherichia coli strain Nissle 1917 attenuates acute gastric lesions induced by stress

Application of a diagnostic-therapeutic procedure using implant-supported dental prosthesis as a preventive therapy for candidiasis of upper gastrointestinal tract in complete denture users

Duodenal mucosal protection by bicarbonate secretion and its mechanisms

Effect of different muscle shortening velocities during prolonged incremental cycling exercise on the plasma growth hormone, insulin, glucose, glucagon, cortisol, leptin and lactate concentrations

Effect of moderate incremental exercise, performed in fed and fasted state on cardio-respiratory variables and leptin and ghrelin concentrations in young healthy men

SU-840, a novel synthetic flavonoid derivative of sophoradin, with potent gastroprotective and ulcer healing activity

Effects of biofeedback training on esophageal peristaltis in amyotrophic lateral sclerosis [ALS] patients with dysphagia

Adaptive cytoprotection by ammonia and urea - urease system in the rat gastric mucosa

Nitric oxide (NO)-releasing aspirin and (NO) donors in protection of gastric mucosa against stress

Neural aspects of ghrelin-induced gastroprotection against mucosal injury induced by noxious agents

Importance of luminal and mucosal zinc in the mechanism of experimental gastric ulcer healing

Interaction between selective cyclooxygenase inhibitors and capsaicin-sensitive afferent sensory nerves in pathogenesis of stress-induced gastric lesions. Role of oxidative stress

Nitric oxide (NO)-releasing aspirin exhibits a potent esophagoprotection in experimental model of acute reflux esophagitis. Role of nitric oxide and proinflammatory cytokines

Lipid peroxidation, reactive oxygen species and antioxidative factors in the pathogenesis of gastric mucosal lesions and mechanism of protection against oxidative stress - induced gastric injury

Interaction of nonsteroidal anti-inflammatory drugs (NSAID) with Helicobacter pylori in the stomach of humans and experimental animals

Role of sensory afferent nerves, lipid peroxidation and antioxidative enzymes in the carbon monoxide-induced gastroprotection against stress ulcerogensis

Protective influence of melatonin against acute esophageal lesions involves prostaglandins, nitric oxide and sensory nerves