Wyniki wyszukiwania

1

Brain-gut axis in ischemic preconditioning of gastro-duodeno-pancreatic cluster

100%

Konturek S. J., Brzozowski T., Pajdo R., Dembinski A., Jaworek J.

Journal of Physiology and Pharmacology. Supplement

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2001

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tom 52

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nr 2

2

Gastric ulcer healing in mouse model of infection with cytotoxin expressing strain of Helicobacter pylori

86%

Brzozowski T., Konturek P. C., Karczewska E., Pajdo R., Ghiara P., Hahn E. G., Konturek S. J.

Journal of Physiology and Pharmacology. Supplement

|

1997

|

tom 48

|

nr 1

3

Sensory nerves and calcitonin gene related peptide in the effect of ischemic preconditioning on acute and chronic gastric lesions induced by ischemia-reperfusion

86%

Pawlik M., Ptak A., Pajdo R., Konturek P. C., Brzozowski T., Konturek S. J.

Journal of Physiology and Pharmacology

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2001

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tom 52

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nr 4,1

Ischemic preconditioning is considered as the most powerful gastroprotective intervention against mucosal lesions and ulcerations but the mechanism of this phenomenon has been little examined. In this study we tested the effects of inactivation of sensory nerves in new rat model combining acute gastric erosions with subsequent ulcers induced by ischemia-reperfusion (I/R). I/R lesions were produced in rats by clamping the celiac artery for 0.5 h followed by 3 h ofreperfusion in rats with intact or inactivated sensory nerves by pretreatment with capsaicin for two weeks before the I/R. The animals were killed at 0 and 3 h and 3 days after I/R and the area of gastric lesions was determined planimetrically, the gastric blood flow (GBF) by H2-gas clearance technique and the plasma levels of gastrin by RIA. Gastric mucosal content of calcitonin gene related peptide (CGRP) was assessed by RIA. Following I/R, gastric erosive lesions occurred after 3 h and these erosive lesions then progressed into gastric ulcers within 3 days in all rats. Sensory-inactivation with capsaicin caused several fold increase in the area of early (at 3 h) acute lesions and later (at 3 d) gastric ulcers induced by I/R. This enhancement of acute and then chronic gastric lesions was accompanied by a significant fall in GBF, an elevation of plasma gastrin and a decrease in mucosal expression of CGRP. Ischemic preconditioning markedly reduced acute lesions and chronic ulcerations induced by I/R and attenuated the changes in plasma gastrin and mucosal CGRP contents but these effects were significantly more pronounced in rats with intact sensory nerves but less in capsaicin-inactivated animals. We conclude that: 1) The I/R resulted in the formation of early acute gastric lesions followed 3 days later by chronic gastric ulcers and this gastric injury was accompanied by an impairment of gastric microcirculation, hypergastrinemia and suppression the gastric mucosal CGRP; 2) Gastric ischemic-preconditioning significantly attenuated both acute mucosal damage and chronic ulcers induced by I/R and this was accompanied by a rise in gastric blood flow; 3) The inactivation of sensory nerves with capsaicin enhanced the formation of I/R-induced acute and chronic gastric lesions and strongly attenuated the gastroprotection afforded by I/R possibly due to the decline in mucosal blood flow and the fall in expression of integrity peptides such as CGRP and 4) The excessive release of gastrin may limit the extent of mucosal lesions observed during progression of gastric erosions into ulcers induced by I/R.

4

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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

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nr 1

5

Ghrelin ameliorates colonic inflammation. Role of nitric oxide and sensory nerves.

73%

Konturek P. C., Brzozowski T., Engel M., Burnat G., Gaca P., Kwiecien S., Pajdo R., Konturek S. J.

Journal of Physiology and Pharmacology

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2009

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tom 60

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nr 2

41-47

Ghrelin is a novel growth hormone (GH)-releasing and orexigenic peptide with anti-inflammatory activities. However, the role of ghrelin in the colonic inflammation is still controversial. The aim of the present study was: 1) to examine the expression of ghrelin and TNF- mRNA in the inflamed colonic mucosa of patients with ulcerative colitis (UC), 2) to analyze the effect of treatment with exogenous ghrelin on the healing of trinitrobenze sulphonic acid (TNBS)-induced colitis in rats, and 3) to assess the effects of ghrelin treatment on mRNA expression for iNOS and protein expression for COX-2 and PPAR in intact colonic mucosa and in that with TNBS-induced colitis. Fifteen patients with UC and fifteen healthy controls were enrolled in this study. Expression of ghrelin and TNF- was assessed by semi-quantitative RT-PCR in the colonic mucosal biopsies from UC patients and healthy controls. In addition, the effect of exogenous ghrelin on healing of TNBS colitis was tested in rats without or with capsaicin-induced functional ablation of sensory nerves. Patients with UC showed a significant upregulation of mRNA for ghrelin and TNF- in colonic mucosa as compared to that observed in healthy controls. The expression of ghrelin correlated with the grade of inflammation and expression of TNF-. In rats the exogenous ghrelin administered daily at a dose of 20 µg/kg i.p. significantly accelerated the healing of TNBS colitis and this effect was accompanied by an increase in mRNA expression for iNOS and protein expression for COX-2 in the colonic mucosa. The protein expression for PPAR, which was down-regulated in rat colonic mucosa after exposure to TNBS as compared to that in intact colonic mucosa, was not significantly influenced by ghrelin treatment. We conclude that 1) patients with UC show an increased mucosal expression of mRNA for ghrelin in the colonic mucosa which could trigger protective response in inflamed colon; and 2) exogenous ghrelin accelerates healing of colonic lesions in animal model of ulcerative colitis via increased release of NO and PGE2 due to an increase in iNOS and COX-2 expression and stimulation of sensory neuropeptides such as CGRP released from sensory afferent endings.

6

Are probiotics effective in the treatment of fungal colonization of the gastrointestinal tract? Experimental and clinical studies

73%

Zwolinska-Wcislo M., Brzozowski T., Mach T., Budak A., Trojanowska D., Konturek P. C., Pajdo R., Drozdowicz D., Kwiecien S.

Journal of Physiology and Pharmacology. Supplement

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2006

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tom 57

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nr 9

35-49

The influence of fungal colonization and probiotic treatment on the course of gastric ulcer (GU) and ulcerative colitis (UC) was not explored. Our studies included: 1) clinical investigation of 293 patients with dyspeptic and ulcer complaints and 72 patients with lower gastrointestinal (GI) tract: 60 patients with UC, 12 with irritable bowel syndrome (IBS) - the control group. Significant fungal colonization (SFC), over 105 CFU/ml was evaluated. Mycological investigation was performed, including qualitative and quantitative examination, according to Muller method, 2) experimental studies in rats included estimation of the influence of inoculation of Candida isolated from human GI tract on the healing process of GU, induced by acetic acid with or without probiotic Lactobacillus acidophilus (106 CFU/ml) introduced intragastrically (i.g.). At 0, 4, 15 and 25 day after ulcer induction. Weight, damage area, gastric blood flow (GBF) (H2 clearance), expression of mRNA for cytokines IL-ß, TNF-alpha (ELISA) were evaluated. Mycology: qualitative and quantitative examination was performed. MPO serum activity was measured. Results of clinical studies: 1) SFC was more frequent in patients with GU: 54.2% of cases and patients with over 5 years history of UC: 33.3% cases. 2) SFC delayed GU healing and influenced the maintenance of clinical symptoms in both diseases. Results of animal studies: 3) In Candida inoculated rats, the GBF was significantly lower than in the vehicle controls (saline administered group). Upregulation of TNF-alpha, IL-1ß was recorded. The GUs were still present till 25 day in all rats inoculated with Candida, in contrast to vehicle group (reduction of ulcer in 92% at day 25). Conclusions: 1) Fungal colonization delays process of ulcer and inflammation healing of GI tract mucosa. That effect was attenuated by probiotic therapy. 2) Probiotic therapy seems to be effective in treatment of fungal colonization of GI tract. 3) Lactobacillus acidophilus therapy shortens the duration of fungal colonization of mucosa (enhanced Candida clearance is associated with IL-4, INF- response).

7

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.

8

Experimental healing of preexisting gastric ulcers induced by hormones controlling food intake ghrelin, orexin-A and nesfatin-1 is impaired under diabetic conditions. A key to understanding the diabetic gastropathy?

73%

Szlachcic A., Majka J., Strzalka M., Szmyd J., Pajdo R., Ptak-Belowska A., Kwiecien S., Brzozowski T.

Journal of Physiology and Pharmacology

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2013

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tom 64

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nr 5

9

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

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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.

10

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

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2014

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tom 65

|

nr 5

11

Esophagoprotective activity of angiotensin-(1-7) in experimental model of acute reflux esophagitis. Evidence of the role of nitric oxide, sensory nerves, hypoxia-inducible factor-1alpha and proinflammatory cytokines

73%

Pawlik M. W., Kwiecien S., Pajdo R., Ptak-Belowska A., Brzozowski B., Krzysiek-Maczka G., Strzalka M., Konturek S. J., Brzozowski T.

Journal of Physiology and Pharmacology

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2014

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tom 65

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nr 6

12

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

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2016

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tom 67

|

nr 5

13

Effects of peripherally and centrally applied ghrelin in the pathogenesis of ischemia-reperfusion induced injury of the small intestine

73%

Pawlik M. W., Obuchowicz R., Biernat J., Szczepanski W., Pajdo R., Kwiecien S., Brzozowski T., Konturek S. J., Pawlik W. W.

Journal of Physiology and Pharmacology

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2011

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tom 62

|

nr 4

14

Protective effect of gastric acid secretion in ammonia induced gastric lesions

73%

Warzecha Z., Dembinski A., Brzozowski T., Ceranowicz P., Niemiec J., Pajdo R., Walocha J., Konturek S. J.

Journal of Physiology and Pharmacology. Supplement

|

1997

|

tom 48

|

nr 1

15

Central and peripheral gastroprotective and secretory activity of histamine and its N-alpha methyl analog

73%

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

Journal of Physiology and Pharmacology. Supplement

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2001

|

tom 52

|

nr 2

16

Ghrelin - a new gastroprotective factor in gastric mucosa

73%

Konturek P. C., Brzozowski T., Pajdo R., Nikiforuk A., Kwiecien S., Harsch I., Drozdowicz D., Hahn E. G., Konturek S. J.

Journal of Physiology and Pharmacology

|

2004

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tom 55

|

nr 2

Ghrelin, a novel peptide expressed in the gastrointestinal tract, especially in the gastric mucosa, exerts several biological activities including the stimulation of appetite and food intake, the stimulation of intestinal motility and the release of growth hormone. The aim of this study was to examine the expression of ghrelin in gastric mucosa after its exposure to ethanol and its effects on gastric lesions induced by ethanol with and without pretreatment with indomethacin. Acute gastric lesions were induced by intragastric administration of 75% ethanol in rats pretreated with saline-vehicle or ghrelin injected intraperitoneally (i.p.) without or with i.p. pretreatment with indomethacin. At the end of experiments, the rats were anesthetized, the stomach was exposed to measure gastric blood flow (GBF), to determine the area of gastric lesions and to take biopsy samples from the oxyntic mucosa for determination of transcripts of ghrelin, tumor necrosis alpha (TNF-alpha) and transforming growth factor alpha (TGFalpha) using RT-PCR and to assess the generation of PGE2 by RIA. Exposure of gastric mucosa to 75% ethanol resulted in numerous mucosal lesions of an area of about 115 mm2 and in the increase of mucosal expression of TNF-alpha, PGE2, TGFalpha and ghrelin with concomitant decrease in GBF. Exogenous ghrelin reduced dose-dependently acute gastric lesions with simultaneous attenuation of GBF and a decrease in the expression of TNF-alpha but not TGFalpha. Pretreatment with indometahcin, which suppressed the generation of PGE2 by about 85%, augmented ethanol-induced gastric lesions and eliminated the ghrelin-induced protection of mucosa against ethanol. We conclude that ghrelin, whose mucosal expression is enhanced after exposure to ethanol, exhibits a strong gastroprotection, at least in part, due to its anti-inflammatory action mediated by prostaglandins.

17

Involvement of cyclooxygenase (COX)-2 products in acceleration of ulcer healing by gastrin and hepatocyte growth factor

73%

Brzozowski T., Konturek P. C., Konturek S. J., Pajdo R., Schuppan D., Drozdowicz D., Ptak A., Pawlik M., Nakamura T., Hahn E. G.

Journal of Physiology and Pharmacology

|

2000

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tom 51

|

nr 4,1

18

Effect of central and peripheral actions of histamine and its metabolite N-alpha methyl histamine on gastric secretion and acute gastric lesions

73%

Kwiecien S., Brzozowski T., Konturek P. C., Konturek S. J., Pawlik M., Pajdo R., Drozdowicz D., Ptak A., Hahn E. G.

Journal of Physiology and Pharmacology

|

2001

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tom 52

|

nr 4,1

Nalpha-methylhistamine (Nalpha-MH) is one of unusual metabolite of histamine that was found in Helicobacter pylori-infected stomach and is believed to interact with specific histamine H1,H2 and H3-receptors to stimulate gastric acid secretion and gastrin release from isolated G-cells but the effects of Nalpha-MH on gastric mucosal integrity have been little studied. This study was designed; 1) to compare the effect of intraperitoneal (i.p.), intracerebroventricular (i.c.v.) and gastric topical (intragastric i.g.) application of exogenous Nalpha-MH with that of standard histamine on gastric secretion in rats equipped with gastric fistula (series A) and 2) to compare the effect of i.c.v. administration of histamine and Nalpha-MH with that of peripheral (i.p. and i.g) application of these amines on gastric lesions induced by 100% ethanol (series B) in rats with or without capsaicin-induced deactivation of sensory nerves. The area of gastric lesions was determined planimetrically, gastric blood flow (GBF) was assessed by H2-gas clearance method and venous blood was collected for determination of plasma gastrin levels by RIA. Nalpha-MH and histamine (0.1—10 mg/kg i.p. or i.g.) dose-dependently increased gastric acid output (series A); whereas i.c.v. administration of histamine or Nalpha-MH inhibited dose-dependently this secretion; the dose attenuating gastric acid output by 50% (ED50) being 4 and 6 µg/kg i.c.v. Both, Nalpha-MH and histamine (2 mg/kg i.p. and i.g.) attenuated significantly the area of gastric lesions induced by 100% ethanol (series B) while producing significant rise in the GBF and plasma immunoreactive gastrin increments. Central application of Nalpha-MH and histamine (0.01—5 µg/kg i.c.v.) inhibited ethanol-induced gastric damage whereas higher doses ranging from 10—100 µg/kg of histamine and Nalpha-MH were significantly less effective. Capsaicin-induced deactivation of sensory nerves by itself augmented significantly ethanol damage and attenuated significantly the protective and hyperemic effects of histamine and its methylated analog applied i.p. but failed to affect significantly those caused by i.c.v. administration of these amines. We concluded that: 1) central histamine and Nalpha-MH inhibits gastric acid secretion and exhibits gastroprotective activity against ethanol in similar manner to that afforded by parenteral and topical histamine and N- MH, 2) central N-alphaMH- and histamine-induced protection involve the enhancement in gastric microcirculation unrelated to neuropeptides released from capsaicin-sensitive afferent nerves, and 3) the major difference between central and peripheral histamine and its methylated analog is the influence on gastric acid secretion which does not appear to play any major role in gastroprotective activity of these agents.

19

Brain-gut axis in gastroprotection by leptin and cholecystokinin against ischemia-reperfusion induced gastric lesions

73%

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

Journal of Physiology and Pharmacology

|

2001

|

tom 52

|

nr 4,1

Leptin, a product of ob gene controlling food intake, has recently been detected in the stomach and shown to be released by CCK and implicated in gastroprotection against various noxious agents but it is unknown whether centrally applied leptin influences ischemia-reperfusion (I/R)-induced gastric erosions that progress into deeper gastric ulcerations. In this study we compared the effects of leptin and CCK-8 applied intracerebroventricularly (i.c.v.) or intraperitoneally (i.p.) on gastric mucosal lesions induced by I/R and topical application of 75% ethanol. Several major series of Wistar rats were used to examine the effects of leptin and CCK applied centrally on gastroprotection against I/R and ethanol in rats with A) vagotomy by cutting of vagal nerves, B) suppression of NO-synthase with L-NNA (20 mg/kg i.p.), C) inactivation of sensory nerves by capsaicin (125 mg/kg s.c.) and D) inhibition of CGRP receptors with CGRP8-37 (100 µg/kg i.p.) applied with or without the i.c.v. pretreatment with leptin or CCK-8. Rats were anesthetized 1 h after ethanol administration or at 3 h and 3 days upon the end of ischemia to measure the gastric blood flow (GBF) and then to determine the area of gastric lesions by planimetry. Blood was withdrawn for the measurement of plasma leptin and gastrin levels by radioimmunoassay (RIA). Leptin (0.1—20 µg/kg i.p.) dose-dependently attenuated gastric lesions induced by 75% ethanol and I/R; the dose reducing these lesions by 50% (ED50) was 8 µg/kg and 6 µg/kg, respectively and this protective effect was similar to that obtained with CCK-8 applied in a standard dose of 10 µg/kg i.p. This protective effect of leptin was accompanied by a significant increase in GBF and plasma gastrin levels whereas CCK-8 increased plasma leptin levels but failed to affect plasma gastrin levels. Leptin and CCK-8 applied i.c.v. in a dose of 625 ng/rat reduced significantly the area of I/R induced gastric lesions and raised the GBF and plasma leptin levels with the extent similar to those achieved with peripheral administration of leptin or CCK-8 (10 µg/kg i.p.). The protective and hyperemic effects of centrally administered leptin or CCK-8 (625 ng/rat i.c.v.) were completely abolished by vagotomy and significantly attenuated by sensory denervation with capsaicin or by CGRP antagonist, CGRP8-37. The pretreatment with L-NNA to inhibit NO-synthase activity attenuated significantly the protective and hyperemic effects of CCK but not those of leptin while capsaicin denervation counteracted leptin-- induced protection and rise in the GBF but attenuated significantly those of CCK. We conclude that: 1) central leptin exerts a potent gastroprotective activity against I/R-induced gastric erosions that progress into deeper gastric lesions and this protection depends upon vagal activity and sensory nerves and involves hyperemia probably mediated by NO and 2) leptin mimics the gastroprotective effect of CCK and may be implicated in the protective and hyperemic actions of this peptide against mucosal damage evoked by I/R.

20

Brain-gut axis in gastroprotection by leptin and cholecystokinin [CCK]

73%

Brzozowski T., Ptak A., Kwiecien S., Sliwowski Z., Pajdo R., Drozdowicz D., Konturek P. C., Konturek S. J., Hahn E. G.

Journal of Physiology and Pharmacology. Supplement

|

2001

|

tom 52

|

nr 2

Ograniczanie wyników

Brain-gut axis in ischemic preconditioning of gastro-duodeno-pancreatic cluster

Gastric ulcer healing in mouse model of infection with cytotoxin expressing strain of Helicobacter pylori

Sensory nerves and calcitonin gene related peptide in the effect of ischemic preconditioning on acute and chronic gastric lesions induced by ischemia-reperfusion

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

Ghrelin ameliorates colonic inflammation. Role of nitric oxide and sensory nerves.

Are probiotics effective in the treatment of fungal colonization of the gastrointestinal tract? Experimental and clinical studies

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

Experimental healing of preexisting gastric ulcers induced by hormones controlling food intake ghrelin, orexin-A and nesfatin-1 is impaired under diabetic conditions. A key to understanding the diabetic gastropathy?

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

Esophagoprotective activity of angiotensin-(1-7) in experimental model of acute reflux esophagitis. Evidence of the role of nitric oxide, sensory nerves, hypoxia-inducible factor-1alpha and proinflammatory cytokines

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

Effects of peripherally and centrally applied ghrelin in the pathogenesis of ischemia-reperfusion induced injury of the small intestine

Protective effect of gastric acid secretion in ammonia induced gastric lesions

Central and peripheral gastroprotective and secretory activity of histamine and its N-alpha methyl analog

Ghrelin - a new gastroprotective factor in gastric mucosa

Involvement of cyclooxygenase (COX)-2 products in acceleration of ulcer healing by gastrin and hepatocyte growth factor

Effect of central and peripheral actions of histamine and its metabolite N-alpha methyl histamine on gastric secretion and acute gastric lesions

Brain-gut axis in gastroprotection by leptin and cholecystokinin against ischemia-reperfusion induced gastric lesions

Brain-gut axis in gastroprotection by leptin and cholecystokinin [CCK]