Wyniki wyszukiwania

1

Effect of sensory nerves and CGRP on the development of caerulein-induced pancreatitis and pancreatic recovery

100%

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

The function of primary sensory neurons is to receive and transmit information from external environment and these neurons are able to release neuromediators from the activated peripheral endings. The aim of this study was to determine the influence of sensory nerves and administration of their mediator — calcitonin gene related peptide (CGRP) on the course of acute pancreatitis (AP). Ablation of sensory nerves was performed by neurotoxic dose of capsaicin (100 mg/kg). Single or repeated episodes of AP were induced by caerulein infusion (10 µg/kg/h for 5 h). Five repeated AP were performed once a week. Capsaicin at the dose which stimulates sensory nerves (0.5 mg/kg/dose) or CGRP (10 µg/kg/dose) was administrated before and during or after single induction of AP, as well as, after each induction of repeated AP. Rats were killed at the time 0, 3 or 9 h after single induction of AP or two weeks after last induction of repeated AP. Ablation of sensory nerves aggravated pancreatic damage in caerulein-induced AP. Treatment with stimulatory doses of capsaicin or CGRP before and during single induction of AP attenuated the pancreatic damage in morphological examination. This effect was also manifested by partial reversion of AP evoked drop in DNA synthesis and pancreatic blood flow (PBF). Administration of CGRP after single AP induction aggravated histologically manifested pancreatic damage. The further decrease in PBF and DNA synthesis was also observed. Animals with five episodes of AP showed almost full pancreatic recovery two weeks after last induction of AP concerning all parameters tested. In stimulatory doses of capsaicin treated rats, we observed the decrease in pancreatic amylase and fecal chymotrypsin activity, as well as, the drop in DNA synthesis. Similar but less pronounced effects were observed after treatment with CGRP. We conclude that effect of sensory nerves and CGRP on AP is two-phase and time dependent. Stimulation of sensory nerves or the administration of CGRP during development of AP exhibits protective effects against pancreatic damage induced by caerulein overstimulation. After induction of AP, persistent activity of sensory nerves and presence of CGRP aggravate pancreatic damage and lead to functional insufficiency typical for chronic pancreatitis.

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

Sensory nerves as modulators of intestinal preconditioning

100%

Obuchowicz R., Pawlik M., Sendur R., Szczepanski W., Biernat J., Pawlik W. W.

Journal of Physiology and Pharmacology. Supplement

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2001

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tom 52

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nr 2

4

Leptin is able to stimulate pancreatic enzyme secretion via activation of duodeno-pancreatic reflex and CCK release

84%

Nawrot-Porabka K., Jaworek J., Leja-Szpak A., Palonek M., Szklarczyk J., Konturek S. J., Pawlik W. W.

Journal of Physiology and Pharmacology. Supplement

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2004

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tom 55

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nr 2

47-57

Leptin, 16- kDa protein produced and secreted from white adipocytes is known to regulate food intake and energy expenditure. Leptin receptors have been detected in the pancreas and it has been shown that systemic application of this protein diminished postprandial pancreatic secretion. Leptin is also produced in the stomach and released into the gastrointestinal lumen but the implication of luminal leptin in the regulation of pancreatic enzyme secretion has not been elucidated. The aim of our study was to evaluate the effects of intraduodenal (i.d.) leptin administration on pancreatic enzyme secretion and to assess the involvent of afferent nerves and CCK in above effects. The secretory studies were carried out on anaesthetized Wistar rats with acute pancreatic fistulae. Leptin was administered to the animals at doses of 0.1 1.0 or 10.0 µg/kg i.d. Tarazepide (2.5 mg/kg i.d.), a CCK1 receptor antagonist, was given to the rats prior to the application of leptin. Rats with capsaicin deactivated sensory nerves were used in part of the study. Samples of pancreatic juice were taken at 15 min intervals to measure the volume flow and protein and amylase concentrations. CCK plasma level was measured by radioimmunoassay (RIA) following administration of leptin to the rats. Intraduodenal administration of leptin (1.0 or 10.0 µg/kg) to the fasted rats significantly and dose-dependently increased pancreatic protein and amylase outputs. Pancreatic secretory responses to leptin were totally abolished by prior capsaicin deactivation of sensory nerves or by pretreatment of the rats with tarazepide. Under basal conditions plasma CCK level averaged about 15.46 ± 1,4 pg/ml. Exogenous leptin, given i.d. at doses of 0.1 1.0 or 10.0 µg/kg i.d. to the rats with intact or capsaicin-deactivated sensory nerves resulted in dose-dependent rise of plasma CCK level, reaching the highest value at the dose of 10.0 µg/kg i.d. We conclude that leptin given i.d. stimulates pancreatic enzyme secretion and this effect could be related to the stimulation of CCK release and activation of duodeno-pancreatic reflexes.

5

Evaluation of the cough reflex and airway reactivity in toluene- and ovalbumin-induced airway hyperresponsiveness

84%

Mokry J., Nosalova G.

Journal of Physiology and Pharmacology. Supplement

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2007

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tom 58

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nr 5

6

Stimulation of sensory nerves and CGRP administration attenuates development pancreatitis evoked by ischemia-reperfusion

84%

Warzecha Z., Dembinski A., Ceranowicz P., Sendur R., Pawlik W. W., Konturek S. J.

Journal of Physiology and Pharmacology. Supplement

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2001

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tom 52

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nr 2

7

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

84%

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

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2007

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tom 58

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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.

8

Influence of sensory nerves and CGRP on the course of experimental pancreatitis and pancreatic regeneration

84%

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

Journal of Physiology and Pharmacology. Supplement

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2001

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tom 52

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nr 2

9

Sensory nerves in central and peripheral control of pancreatic integrity by leptin and malatonin

84%

Jaworek J., Bonior J., Leja-Szpak A., Nawrot K., Kot M., Tomaszewska R., Stachura J., Pawlik W. W., Konturek S. J.

Journal of Physiology and Pharmacology

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2002

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tom 53

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nr 1

Central nervous system affects pancreatic secretion of enzymes however,the neural modulation of acute pancreatitis has not been investigated.Leptin and melatonin have been recently reported to affect the inflammatory response of various tissues.The identification of specific receptors for both peptides in the pancreas suggests that leptin and melatonin could contribute to the pancreatic protection against inflammation.The aim of this study was:1/to compare the effect of intracerebroventricular (i.c.v.)or intraperitoneal (i.p.) administration of leptin or melatonin on the course of caerulein-induced pancreatitis (CIP) in the rat,2/to examine the involvement of sensory nerves (SN)and calcitonin gene-related peptide (CGRP)in pancreatic protection afforded by leptin or melatonin,3/to assess the effect of tested peptides on lipid peroxidation products (MDA +4-HNE)in the pancreas of CIP rats,4/to investigate the influence of leptin or melatonin on nitric oxide (NO)release from isolated pancreatic acini and 5/to determine the effects of caerulein and leptin on leptin receptor gene expression in these acini by RT-PCR.CIP was induced by subcutaneous (s.c.)infusion of caerulein (25 µg/kg)to the conscious rats,confirmed by the significant increases of pancreatic weight and plasma amylase and by histological examination.This was accompanied in marked reduction of pancreatic blood flow and significant rise of MDA +4-HNE in the pancreas.Leptin or melatonin were administered i.p.or i.c.v.30 min prior to the start of CIP.Deactivation of SN was produced by s.c.capsaicin (100 mg/kg).An antagonist of CGRP,CGRP8-37 (100 µg/kg i.p.),was given together with leptin or melatonin to the CIP rats.MDA +4-HNE was measured using LPO commercial kit.NO was determined using the Griess reaction.Pretreatment of CIP rats with i.p.leptin (2 or 10 µg/kg)or melatonin (10 or 50 mg/kg)significantly attenuated the severity of CIP.Similar protective effects were observed following i.c.v.application of leptin (0.4 or 2 µg/rat)but not melatonin (10 or 40 µg/rat)to the CIP rats.Capsaicin deactivation of SN or administration of CGRP8-37 abolished above beneficial effects of leptin on CIP,whereas melatonin-induced protection of pancreas was unaffected.Pretreatment with i.p.melatonin (10 or 50 mg/kg),but not leptin,significantly reduced MDA +4-HNE in the pancreas of CIP rats.Leptin (10–9 -10–6 M)but not melatonin (10–8 -10–5 M)significantly stimulated NO release from isolated pancreatic acini.Leptin receptor gene expression in these acini was significantly increased by caerulein and leptin. We conclude that 1/central or peripheral pretreatment with leptin protects the pancreas against its damage induced by CIP,whereas melatonin exerts its protective effect only when given i.p.,but not following its i.c.v.adminstration,2/activation of leptin receptor in the.pancreatic acini appears to be involved in the beneficial effects of leptin on acute pancreatitis, 3/the protective effects of leptin involve sensory nerves,CGRP and increased generation of NO whereas melatonin-induced protection of the pancreas depends mainly on the antioxidant local effect of this indole,and scavenging of the radical oxygen species in the pancreatic tissue.

10

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.

11

Role of prostaglandins, sensory nerves, nitric oxide and growth factors in gastric adaptation to topical irritants

84%

Konturek S. J., Brzozowski T., Konturek J. W., Domschke W.

Journal of Physiology and Pharmacology. Supplement

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1993

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tom 44

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nr 2

12

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The influence of sensory nerves and CGRP on the pancreatic regeneration after repeated episodes of acute pancreatitis in rats

84%

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

Journal of Physiology and Pharmacology

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2000

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tom 51

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nr 3

13

Importance of brain-gut axis in the gastroprotection induced by gastric and remote preconditioning

84%

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

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 1,2

Limitation of the damage to the organs such as heart, liver, intestine, stomach and brain by an earlier brief complete occlusion of their arteries is defined as ischemic preconditioning (IP). No study so for has been undertaken to check whether brain-gut axis is involved in the gastroprotection exhibited by gastric IP or in that induced by repeated brief episodes of ischemia of remote organs such as heart and liver. This study was designed to determine the possible involvement of vagal and sensory afferent nerves, in the mechanism of gastric and remote organ IP on the gastric mucosa in rats exposed to prolonged ischemia-reperfusion with or without functional ablation of sensory nerves by capsaicin or in those with removed vagal innervation by vagotomy. This gastric IP was induced by short ischemia episodes (occlusion of celiac artery 1-5 times for 5 min) applied 30 min before subsequent ischemia followed by 3 h of reperfusion (I/R) and compared with remote IP induced by occlusion of left descending coronary artery or hepatic artery plus portal vein. The area of gastric lesions was determined by planimetry, gastric blood flow (GBF) was measured by H2-gas clearance method and mucosal biopsy samples were taken for the assessment of calcitonin gene-related peptide (CGRP) by RIA. Exposure of gastric mucosa to standard 3 h of I/R produced numerous gastric lesions and significant fall in the GBF and mucosal CGRP content. Two 5 min short ischemic episodes by occlusion of coronary or hepatic arteries, significantly reduced gastric damage induced by I/R with the extent similar to that exhibited by two short (5 min) episodes of gastric ischemia. These protective effects of gastric and remote IPs were accompanied by a restoration of the fall in the CGRP content caused by I/R alone. Protection and hyperemia induced by gastric IP were significantly attenuated in capsaicin-denervated or vagotomized animals and completely removed in those exposed to the combination of vagotomy and capsaicin-denervation. The IP-induced protection and hyperemia were restored by the administration of exogenous CGRP to gastric IP in capsaicin-treated animals. Gastroprotective and hyperemic actions of remote IP were markedly diminished in capsaicin-denervated rats and in those subjected to vagotomy. We conclude that brief ischemia in remote organs such as heart and liver protects gastric mucosa against gastric injury induced by I/R as effectively as gastric IP via mechanism involving both vagal and sensory nerves releasing vasodilatatory mediators such as CGRP.

14

Ischemic preconditioning attenuates gastric ischemia-reperfusion injury through involvement of glucocorticoids

67%

Bobryshev P., Bagaeva T., Filaretova L.

Journal of Physiology and Pharmacology. Supplement

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2009

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tom 60

|

nr 7

15

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

67%

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

|

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.

16

Melatonin as modulator of pancreatic enzyme secretion and pancreatoprotector

67%

Jaworek J., Nawrot-Porabka K., Leja-Szpak A., Bonior J., Szklarczyk J., Kot M., Konturek S. J., Pawlik W. W.

Journal of Physiology and Pharmacology. Supplement

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2007

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tom 58

|

nr 6

17

Mucosal strengthening activity of central and peripheral melatonin in the mechanism of gastric defense

67%

Brzozowska I., Ptak-Belowska A., Pawlik M., Bajdo R., Drozdowicz D., Konturek S. J., Pawlik W. W., Brzozowski T.

Journal of Physiology and Pharmacology. Supplement

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2009

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tom 60

|

nr 7

18

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

|

nr 3

149-162

19

Hydrogen sulfide-induced colonic mucosal cytoprotection involves T-type calcium channel-dependent neuronal excitation in rats

67%

Matsunami M., Kirishi S., Okui T., Kawabata A.

Journal of Physiology and Pharmacology

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2012

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tom 63

|

nr 1

20

Role of sensory nerves in gastroprotective effect of anandamide in rats

67%

Warzecha Z., Dembinski A., Ceranowicz P., Dembinski M., Cieszkowski J., Kownacki P., Konturek P. C.

Journal of Physiology and Pharmacology

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2011

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tom 62

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nr 2

Previous studies have shown that stimulation of cannabinoid 1 (CB1) receptor protects the gastric mucosa against stress-induced lesion. Aim of the present study was to examine the influence of anandamide on lipid peroxidation and antioxidant defense system in gastric mucosa and the role of sensory nerves in gastroprotective effects of cannabinoids. Studies were performed on rats with intact or ablated sensory nerves (by neurotoxic doses of capsaicin). Gastric lesions were induced by water immersion and restrain stress (WRS). Anandamide was administered at the dose of 0.3, 1.5 or 3.0 µmol/kg, 30 min before exposure to WRS. CB1 receptor antagonist, AM251 (4.0 µmol/kg) was administered 40 min before WRS. WRS induced gastric lesions associated with the decrease in gastric blood flow, mucosal DNA synthesis and mucosal activity of superoxide dismutase (SOD). Serum level of interleukin-1ß (IL-1ß) and mucosal level of malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) were increased. Administration of anandamide reduced the ulcers area, generation of MDA+4-HNE and serum level of IL-1ß, and this effect was associated with the reduction in the WRS-induced decrease in gastric mucosal blood flow, mucosal DNA synthesis and SOD activity. Ablation of sensory nerves increased the area of ulcers, serum level of IL-1ß and mucosal content of MDA+4-HNE, whereas mucosal DNA synthesis, SOD activity and blood flow were additionally decreased. In rats with ablation of sensory nerves, administration of anandamide at the high doses (1.5 and 3.0 µmol/kg) partly reduced deleterious effect of WRS on gastric mucosa, but this effect was weaker than in animals with intact sensory nerves. Low dose of anandamide (0.3 µmol/kg) was ineffective in the protection of gastric mucosa against the WRS-induced lesions in rats with ablation of sensory nerves. In rats with intact sensory nerves and exposed to WRS, administration of AM251 exhibited deleterious effect. In rats with ablation of sensory nerves and exposed to WRS, AM251 failed to affect mucosal injury in the stomach. We conclude that anandamide reduces the mucosal oxidative stress and exhibits gastroprotective effect against WRS-induced ulcers. These effects are partly mediated by sensory nerves.

Ograniczanie wyników

Effect of sensory nerves and CGRP on the development of caerulein-induced pancreatitis and pancreatic recovery

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

Sensory nerves as modulators of intestinal preconditioning

Leptin is able to stimulate pancreatic enzyme secretion via activation of duodeno-pancreatic reflex and CCK release

Evaluation of the cough reflex and airway reactivity in toluene- and ovalbumin-induced airway hyperresponsiveness

Stimulation of sensory nerves and CGRP administration attenuates development pancreatitis evoked by ischemia-reperfusion

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

Influence of sensory nerves and CGRP on the course of experimental pancreatitis and pancreatic regeneration

Sensory nerves in central and peripheral control of pancreatic integrity by leptin and malatonin

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

Role of prostaglandins, sensory nerves, nitric oxide and growth factors in gastric adaptation to topical irritants

The influence of sensory nerves and CGRP on the pancreatic regeneration after repeated episodes of acute pancreatitis in rats

Importance of brain-gut axis in the gastroprotection induced by gastric and remote preconditioning

Ischemic preconditioning attenuates gastric ischemia-reperfusion injury through involvement of glucocorticoids

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

Melatonin as modulator of pancreatic enzyme secretion and pancreatoprotector

Mucosal strengthening activity of central and peripheral melatonin in the mechanism of gastric defense

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

Hydrogen sulfide-induced colonic mucosal cytoprotection involves T-type calcium channel-dependent neuronal excitation in rats

Role of sensory nerves in gastroprotective effect of anandamide in rats