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Protective effect of gastric acid secretion in ammonia induced gastric lesions

100%

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

Journal of Physiology and Pharmacology. Supplement

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1997

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tom 48

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nr 1

2

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

100%

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.

3

L-carnitine protects gastric mucosa by decreasing ischemia-reperfusion induced lipid peroxidation

100%

Derin N., Izgut-Uysal V. N., Agac A., Aliciguzel Y., Demir N.

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 3

Studies have shown that reactive oxygen metabolites and lipid peroxidation play important roles in ischemia-reperfusion injury in many organs such as heart, brain and stomach. The aim of this study is to evaluate the antioxidant effect of L-carnitine on gastric mucosal barrier, lipid peroxidation and the activities of antioxidant enzymes in rat gastric mucosa subjected to ischemia-reperfusion injury. Rats were subjected to 30 min of ischemia followed by 60 min of reperfusion. L-carnitine (100 mg/kg), was given to rats intravenously five minutes before the ischemia. In our experiment, lesion index, thiobarbituric acid reactive substances, prostaglandin E2 and mucus content in gastric tissue were measured. The results indicated that the lesion index and the formation of thiobarbituric acid reactive substances increased significantly with the ischemia-reperfusion injury in the gastric mucosa. L-carnitine treatment reduced these parameters to the values of sham operated rats. The tissue catalase and superoxide dismutase activities and prostaglandin E2 production decreased significantly in the gastric mucosa of rats exposed to ischemia-reperfusion. L-carnitine pretreatment increased the tissue catalase activity and prostaglandin E2 to the levels of sham-operated rats but did not change superoxide dismutase activity. There were no significant difference in glutathione peroxidase activity and mucus content between the groups in the gastric mucosa. In summary, L-carnitine pretreatment protected gastric mucosa from ischemia-reperfusion injury by its decreasing effect on lipid peroxidation and by preventing the decrease in prostaglandin E2 content of gastric mucosa.

4

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Role of polyamines in gastroprotection induced by epidermal growth factor

84%

Brzozowski T., Drozdowicz D., Majka J., Polonczyk-Pytko J., Konturek S. J.

Journal of Physiology and Pharmacology

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1991

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tom 42

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nr 2

Polyamines have been shown to stimulate cellular growth and differentiation, though their role in the prevention of acute gastric lesion induced by various noxious agents has been little studied. Epidermal growth factor (EGF) exhibits gastroprotective and ulcer healing properties due to its potent mitogenic and growth promoting action. This study was designed to compare the gastroprotective effects of spermine and EGF against gastric damage induced by absolute ethanol, acidified aspirin and stress and to determine the role of endogenous polyamines in EGF-induced gast- troprotection. Spermine and EGF significantly reduced the lesions induced by all three ulcerogens. Oral administration of spermine or subcutaneous infusion of EGF in 24 h fasted rats with chronic gastric fistula resulted in similar inhibition of gastric acid and pepsin secretion. Pretreatment with difluoromethylornithine (DFMO), an irreversible inhibitor of ornithine decarboxylase (ODC), a hey enzyme in the biosynthesis of polyamines, did not affect ethanol lesions, but reversed the protective effect EGF but not spermine, against ethanol. This finding indicates that polyamines mediate, at least in part, EGF-induced gastroprotection. In tests with oral administration of aminoguanidine that is known to suppress the activity of diamino-oxidase (DAO) and to inhibit the degradation of polyamines, EGF showed a markedly enhanced gastroprotective activity against ethanol damage. Since indomethacin failed to affect the gastroprotective effects of spermine and EOF and neither of these agents influenced the mucosal generation of PGE₂ in intact or injured gastric mucosa, we conclude that prostaglandins are not the major factors in spermine- and EGF-induced gastroprotection. This study demonstrates that polyamines are highly effective against gastric lesions induced by various ulcerogens and that they act as primary mediators of EGF-induced gastroprotection.

5

Solcoseryl in prevention of stress-induced gastric lesions and healing of chronic ulcers

84%

Konturek S. J., Drozdowicz D., Pytko-Polonczyk J., Brzozowski T., Bielanski W.

Journal of Physiology and Pharmacology

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1991

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tom 42

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nr 1

Solcoseryl, a deproteinized extract of calf blood, protects the gastric mucosa against various topical irritants and enhances the healing of chronic gastric ulcerations but the mechanisms of these effects have been little studied. This study was designed to elucidate the active principle in Solcoseryl and to determine the role of prostaglandisn (PG) and polyamines in the antiulcer properties of this agent. Using both, the radioimmunoassay and radioreceptor assay, EGF-like material was detected in Solcoseryl preparation. Solcoseryl given s. c. prevented the formation of stress-indused gastric lesions and this was accompanied by an increase in the generation of PGE2 in the gastric mucosa. Similar effects were obtained with EGF. Pre treatment with indomethacin, to suppress mucosal generation of prostaglandins (PG), greatly augmented stress- induced gastric ulcerations and antagonized the protection exerted by both Solcoseryl and EGF. Solcoseryl, like EGF, enhanced the healing of chronic gastroduodenal ulcerations. This effect was abolished by the pretreatment with difluoro- methylomithine, an inhibitor of ornithine decarboxylas, the key enzyme in the biosynthesis of polyamines. The healing effects of Solcoseryl and EGF was also reduced by prednisolone which decreased the angiogenesis in the granulation tissue in the ulcer area. These results indicate that Solcoseryl 1. contains EGF-like material, 2. displays the protective and ulcer healing effects similar to those of EGF and involving both PG and polyamines and 3. acts via similar mechanism as does EGF.

6

Roles of endogenous prostaglandins and cyclooxygenase isozymes in mucosal defense of inflamed rat stomach

84%

Takeeda M., Hayashi Y., Yamato M., Murakami M., Takeuchi K.

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 1,2

Endogenous prostaglandins (PGs) are involved in adaptive gastric protection against acute injury, and cyclooxygenase (COX)-1 is responsible for the production of PGs in this phenomenon. In the present study, we examined the effect of various COX inhibitors on gastric ulcerogenic and acid secretory responses following daily exposure of the stomach to iodoacetamide (IA) and investigated the role for COX isozyme in gastric protection under subchronic mucosal irritation. Gastric mucosal irritation was induced by addition of 0.1% IA to drinking water, and the gastric mucosa was examined on the 6th day. Indomethacin (5 mg/kg) or SC-560 (selective COX-1 inhibitor, 5 mg/kg) or rofecoxib (selective COX-2 inhibitor, 5 mg/kg) was given p.o. twice 24 hr and 3 hr before the termination of IA treatment. Giving IA in drinking water for 5 days produced minimal damage in the stomach. The damage was significantly worsened by indomethacin, resulting in hemorrhagic lesions. Both SC-560 and rofecoxib also aggravated such lesions, although the effect of rofecoxib was more pronounced. Treatment with IA decreased acid secretion in pylorus-ligated stomachs, and this change was significantly reverted by indomethacin as well as SC-560 and rofecoxib. Mucosal PGE2 content was increased following IA treatment, with apparent expression of COX-2 mRNA in the stomach, and the increased PGE2 production was significantly suppressed by SC-560 and rofecoxib as well as indomethacin. These results suggest that endogenous PGs derived from both COX-1 and COX-2 are involved in the mucosal defense of the inflamed stomach, partly by decreasing acid secretion and contribute to maintaining the mucosal integrity under such conditions.

7

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

84%

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

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2001

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tom 52

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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.

8

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

67%

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

9

The healing of NSAID-induced gastric lesions may be followed by small intestinal and cardiovascular side effects

67%

Filaretova L. P., Bagaeva T. R., Morozova O. Y., Zelena D.

Journal of Physiology and Pharmacology

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2011

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tom 62

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nr 6

10

Melatonin in gastroprotection against stress-induced acute gastric lesions and in healing of chronic gastric ulcers

67%

Konturek S. J., Konturek P. C., Brzozowski T.

Journal of Physiology and Pharmacology. Supplement

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2006

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tom 57

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nr 5

51-66

The degree of gastric damage following to exposition of the mucosa to noxious agents depends upon a balance between the factors promoting this damage and those activating the natural defense mechanisms. Recent findings, presented in this review, provide evidence that melatonin prevents the formation of acute gastric lesions induced by stress and accelerates healing of chronic gastric ulcers due to increase in the activity of nitric oxide (NO) synthase (NOS)-NO and cyclooxygenase (COX)-prostaglandin E2 (PGE2) systems resulting in the increase of mucosal blood flow and mucosal integrity. Melatonin is produced and released into the circulation by the pineal gland and, in many times larger amounts, by the gastrointestinal tract. Due to its anti-inflammatory and anti-oxidant properties, melatonin may be one of the most efficient protective factors preventing the development of acute gastric damage and accelerating healing of chronic gastric ulcers probably due to reduction in proinflammatory cytokine production, scavenging of the radical oxygen species and activation of COX-PG and NOS-NO systems as well as stimulating the afferent sensory nerves in the brain-gut axis.

11

Gastroprotective and cicatrizing activity of the Ziziphus joazeiro Mart. leaf hydroalcoholic extract

67%

Brito S. M. O., Martins A. O. B. P. B., De Oliveira M. R. C., Vidal C. S., De Lacerda Neto L. J., Ramos A. G. B., Da Gruz L. P., Nascimento E. A., Da Costa J. G. M., Coutinho H. D. M., Quintans-Junior L. J., De Menezes I. R. A.

Journal of Physiology and Pharmacology

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2020

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tom 71

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nr 3

12

Asymmetric dimethylarginine, an endogenous inhibitor of nitric oxide synthase, interacts with gastric oxidative metabolism and enhances stress-induced gastric lesions

67%

Kwiecien S., Ptak-Bielowska A., Krzysiek-Maczka G., Targosz A., Jasnos K., Magierowski M., Szczyrk U., Brzozowski B., Konturek S. J., Konturek P. C., Brzozowski T.

Journal of Physiology and Pharmacology

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2012

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tom 63

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nr 5

13

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

67%

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

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2001

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tom 52

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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.

14

Spirocerca lupi isolated from gastric lesions in foxes (Vulpes vulpes) in Sicily (Italy)

59%

Ferrantelli V., Riili S., Vicari D., Percipalle M., Chetta M., Monteverde V., Gaglio G., Giardina G., Usai F., Poglayen G.

Polish Journal of Veterinary Sciences

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2010

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tom 13

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nr 3

15

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

59%

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

|

nr 6

16

Calcitonin gene-related peptide can attenuate or augment pancreatic damage in caerulein-induced pancreatitis in rats

59%

Warzecha Z., Dembinski A., Ceranowicz P., Konturek P. C., Stachura J., Tomaszewska R., Konturek S. J.

Journal of Physiology and Pharmacology

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1999

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tom 50

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nr 1

Ograniczanie wyników

Protective effect of gastric acid secretion in ammonia induced gastric lesions

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

L-carnitine protects gastric mucosa by decreasing ischemia-reperfusion induced lipid peroxidation

Role of polyamines in gastroprotection induced by epidermal growth factor

Solcoseryl in prevention of stress-induced gastric lesions and healing of chronic ulcers

Roles of endogenous prostaglandins and cyclooxygenase isozymes in mucosal defense of inflamed rat stomach

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

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

The healing of NSAID-induced gastric lesions may be followed by small intestinal and cardiovascular side effects

Melatonin in gastroprotection against stress-induced acute gastric lesions and in healing of chronic gastric ulcers

Gastroprotective and cicatrizing activity of the Ziziphus joazeiro Mart. leaf hydroalcoholic extract

Asymmetric dimethylarginine, an endogenous inhibitor of nitric oxide synthase, interacts with gastric oxidative metabolism and enhances stress-induced gastric lesions

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

Spirocerca lupi isolated from gastric lesions in foxes (Vulpes vulpes) in Sicily (Italy)

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

Calcitonin gene-related peptide can attenuate or augment pancreatic damage in caerulein-induced pancreatitis in rats