A Dembiński

Jagiellonian University, Cracovia, Lesser Poland Voivodeship, Poland

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Publications (156)685.96 Total impact

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    ABSTRACT: Previous studies have shown that treatment with ghrelin exhibits protective and therapeutic effects in the gut. Aim of our present investigation was to examine the influence of ghrelin administration on the healing of ethanol-induced gastric ulcers and determine the role of cyclooxygenase-1 and cyclooxygenase-2 in this effect. Our studies were performed on male Wistar rats. Gastric ulcers were induced by intragastric administration of 75% ethanol. Ghrelin alone or in combination with cyclooxygenase inhibitors was administered twice, 1 and 13 hours after ethanol application. Cyclooxygenase-1 (COX-1) inhibitor (SC-560, 10 mg/kg/dose) or COX-2 inhibitor (celecoxib, 10 mg/kg/dose) were given 30 min prior to ghrelin. Twelve or 24 hours after administration of ethanol, rats were anesthetized and experiments were terminated. The study revealed that administration of ethanol induced gastric ulcers in all animals and this effect was accompanied by the reduction in gastric blood flow and mucosal DNA synthesis. Moreover induction of gastric ulcer by ethanol significantly increased mucosal expression of mRNA for COX-2, IL-1β and TNF-α. Treatment with ghrelin significantly accelerated gastric ulcer healing. Therapeutic effect of ghrelin was associated with significant reversion of the ulcer-evoked decrease in mucosal blood flow and DNA synthesis. Ghrelin administration also caused the reduction in mucosal expression of mRNA for IL-1β and TNF-α. Addition of SC-560 slightly reduced the therapeutic effect of ghrelin in the healing of ethanol-induced ulcer and the ulcer area in rats treated SC-560 plus ghrelin was significantly smaller than that observed in rats treated with saline or SC-560 alone. Pretreatment with celecoxib, a COX-2 inhibitor, abolished therapeutic effect of ghrelin. We concluded that treatment with ghrelin increases healing rate of gastric ulcers evoked by ethanol and this effect is related to improvement in mucosal blood flow, an increase in mucosal cell proliferation, and reduction in mucosal expression of proinflammatory cytokines. Ghrelin is able to reverse a deleterious effect of COX-1 inhibitor on healing of ethanol-induced gastric ulcers. Activity of COX-2 is necessary for the therapeutic effect of ghrelin in healing of ethanol-induced gastric ulcers.
    Journal of physiology and pharmacology: an official journal of the Polish Physiological Society 02/2014; 65(1):95-106. · 2.48 Impact Factor
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    ABSTRACT: Ghrelin exhibits protective and therapeutic effect in different parts of the gastrointestinal tract. The aim of the present study was to examine the influence of ghrelin administration on the healing of oral ulcers in rats with intact salivary gland and in sialoadenectomized rats. Gingival and lingual ulcers were induced by acetic acid. After induction of ulcers, rats were treated with saline or ghrelin for six days. In rats with intact salivary glands and induction of oral ulcers, administration of ghrelin significantly increased the healing rate of these ulcers. This result was associated with a significant increase in mucosal blood flow and cell proliferation, and a decrease in concentration of pro-inflammatory interleukin-1β in gingival and lingual mucosa. Sialoadenectomy decreased cell proliferation and increased concentration of pro-inflammatory interleukin-1β in oral mucosa, as well as reduced the healing rate of gingival and lingual ulcers. Administration of ghrelin reversed deleterious effect of sialoadenectomy and increased the healing rate of oral ulcers above a value observed in rats with intact salivary glands. Conclusions: Treatment with ghrelin accelerates healing of oral ulcers in salivary glands-intact rat, as well as in rats with reduced salivary secretion evoked by sialoadenectomy. Mechanisms of beneficial effects of ghrelin administration involve an increase in mucosal blood flow and cell proliferation, as well as a reduction in local inflammation.
    Journal of physiology and pharmacology: an official journal of the Polish Physiological Society 10/2013; 64(5):657-68. · 2.48 Impact Factor
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    ABSTRACT: Previous studies have shown that tachykinins, the largest family of neuropeptides, affect the development of mucosal damage in the stomach and colon. The aim of the study was to assess the influence of tachykinins receptors antagonists on the development of the mucosa injury in the proximal and distal jejunum. Mucosal damage was induced by administration of non-steroidal anti inflammatory drugs (NSAIDs), indomethacin, celecoxib or combination of indomethacin plus celecoxib given intragastrically. NK-1 receptor antagonist (SR 140333), NK-2 receptor antagonist (SR 48968) and NK-3 receptor antagonist (SR 142801) were administered intraperitoneally twice, 30 min before treatment with NSAID and again 24 h later, 30 min before the end of the experiment. Administration of indomethacin, a relatively selective inhibitor for cyclooxygenase-1 (COX-1), induced mucosal lesions in the jejunum. Lesions area in the distal jejunum was 8-fold bigger than in the proximal jejunum. This effect was associated with a significant reduction in mucosal blood flow and an increase in mucosal concentration of pro-inflammatory interleukin-1beta (IL-1beta). Celecoxib, selective inhibitor for COX-2 failed to induce mucosal lesions and did not affect the mucosal blood flow and IL-1beta concentration in the proximal and distal jejunum. In rats treated with a combination of indomethacin plus celecoxib, ulcers reached maximal area. This effect was associated with the highest concentration of mucosal IL-1beta and maximal reduction in mucosal blood flow. Administration of NK-1 receptor antagonist, SR 140333 reduced jejunal damage induced by indomethacin given alone or in combination with celecoxib. This effect was associated with significant reduction in mucosal concentration of IL-1beta. Effect of SR 140333 on mucosal blood flow was statistically insignificant. Neither NK-2 nor NK-3 receptor inhibitor affected mucosal blood flow, IL-1beta concentration area of NSAIDs-induced mucosal damage in the jejunum. Blockade of NK-1 receptor protects the jejunum against NSAIDs-induced mucosal injury and reduces local inflammation. This observation indicates the involvement of endogenous tachykinins in deleterious effects of NSAID.
    Przegla̧d lekarski 01/2013; 70(2):48-52.
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    ABSTRACT: Previous studies have shown that pancreatic ischemic preconditioning or heparin, applied before induction of acute pancreatitis inhibit the development of this disease and accelerate pancreatic recovery. The aim of the study was to determine the influence of treatment with heparin on protective effect of ischemic preconditioning (IP) in ischemia/reperfusion-induced acute pancreatitis. Heparin was administered twice, before and during induction of acute pancreatitis. IP was performed by short-term clamping of celiac artery, 30 min before induction of acute pancreatitis. Acute pancreatitis was induced in rats by clamping of inferior splenic artery for 30 min followed by reperfusion. Rats were sacrificed after 6-h and 24-h reperfusion. Results: IP applied alone caused a mild pancreatic damage associated with a limited increase in plasma amylase activity, concentration of pro-inflammatory interleukin-1β and plasma level of D-dimer. Pretreatment with heparin or IP applied alone reduced the severity of acute pancreatitis. Both these procedures caused a similar reduction in plasma lipase, amylase and interleukin-1β, as well as in histological signs of pancreatic damage. These changes were associated with partial reversion of the pancreatitis-evoked fall of pancreatic blood flow and DNA synthesis. Combination of heparin plus IP reduced the protective effect of heparin or IP applied alone. It was manifested by an increase in pancreatic damage and plasma level of lipase, amylase and interleukin-1β, as well as by reduction in pancreatic DNA synthesis and plasma concentration of D-dimer and interleukin-10. Conclusions: heparin abolishes the protective effect of ischemic preconditioning in ischemia reperfusion-induced pancreatitis. This observation suggests that initial clot formation is necessary to induce pancreatic protection by IP.
    Journal of physiology and pharmacology: an official journal of the Polish Physiological Society 09/2012; 63(4):355-65. · 2.48 Impact Factor
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    ABSTRACT: Previous studies have shown that administration of ghrelin exhibits protective and therapeutic effects in the gut. The aim of the present investigation was to examine the influence of ghrelin administration on the course of cysteamine-induced duodenal ulcers, as well as effects on mucosal production of oxygen free radicals and duodenal antioxidant defense. Duodenal ulcers were induced in male Wistar rats by cysteamine administered intragastrically at the dose of 200 mg/kg in 1 ml of saline, 3 times at 4-h intervals. Starting 24 h after the first dose of cysteamine, rats were treated intraperitoneally twice a day with saline or ghrelin given at the dose of 4, 8 or 16 nmol/kg/dose. Seven days after administration of the first dose of cysteamine, the study was terminated. Induction of ulcers by cysteamine was accompanied by a reduction in duodenal blood flow, mucosal DNA synthesis and mucosal activity of superoxide dismutase (SOD); whereas mucosal concentration of interleukin-1β and malonyldialdehyde (MDA - an index of lipid peroxidation) were increased. Treatment with ghrelin increased healing rate of duodenal ulcers and enhanced duodenal blood flow, mucosal DNA synthesis and mucosal activity of SOD, and reduced mucosal concentration of interleukin-1β and MDA. Treatment with ghrelin increases the healing rate of duodenal ulcers and this effect is related, at least in part, to improvement of duodenal mucosal blood flow, mucosal cell proliferation and antioxidant defense, as well as being related to reduction in mucosal oxidative stress and inflammatory response.
    Medical science monitor: international medical journal of experimental and clinical research 04/2012; 18(5):BR181-7. · 1.22 Impact Factor
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    ABSTRACT: Apelin is known to stimulate cholecystokinin (CCK) and inhibit insulin release, however the mechanisms on pancreatic secretion remain unclear. The present study aimed to determine the expression of apelin and apelin receptor in the pancreas by immunofluorescence studies and the effect of exogenous apelin on the secretion of pancreatic juice in anesthetized rats. Pancreatic-biliary juice (P-BJ) was collected from Wistar rats treated with apelin (10, 20 and 50 nmol/kg b.w., boluses given every 30 min intravenously or intraduodenaly). The same apelin doses were administered to rats subjected to intraduodenal tarazapide, capsaicin or vagotomy. Pancreatic blood flow was measured by a laser doppler flowmeter. Direct effects of apelin were tested on dispersed acinar cells. Apelin receptor was expressed on acinar cells, pancreatic duct and islets cells, whereas apelin in pancreatic acini, but not in the islets. Intravenous apelin decreased P-BJ volume, protein and trypsin outputs in a dose-dependent manner. In contrast, intraduodenal apelin stimulated P-BJ secretion. Pharmacological block of mucosal CCK(1) receptor by tarazepide, vagotomy and capsaicin pretreatment abolished the effects of intravenous and intraduodenal apelin on P-BJ volume, protein and tryspin outputs. Apelin decreased the pancreatic blood flow. Apelin at 10(-6) M increased the release of amylase from non-stimulated and CCK-8-stimulated acinar cells. In conclusion, apelin can affect the exocrine pancreas through a complex mechanism involving local blood flow regulation and is driven by vagal nerves.
    Journal of physiology and pharmacology: an official journal of the Polish Physiological Society 02/2012; 63(1):53-60. · 2.48 Impact Factor
  • Z Warzecha, A Dembinski
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    ABSTRACT: Ghrelin, a peptide predominantly produced in the stomach exhibits numerous physiological functions, including stimulation of growth hormone release, food intake and gastric empting, and regulation of energy expenditure. This peptide exhibits also some protective and healing-promoting effects. This review summarizes the recent findings concerning animal and human data showing protective and therapeutic effects of ghrelin in the gut.
    Current Medicinal Chemistry 01/2012; 19(1):118-25. · 3.72 Impact Factor
  • Pancreatology 01/2012; 12(6):509. · 2.04 Impact Factor
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    ABSTRACT: Previous studies have shown that administration of obestatin exhibits a protective effect in the pancreas, attenuating the development of acute pancreatitis. The aim of the present study was to investigate the influence of obestatin administration on the healing of chronic gastric ulcers. Chronic gastric ulcers were induced in rats by 100% acetic acid applied to the serosal surface of the gastric wall. Obestatin was given twice a day intraperitoneally at the dose of 4, 8 or 16 nmol/kg/dose for 6 days. Six days after induction of ulcers, rats were anesthetized and the stomach was exposed for measurement of gastric blood flow and ulcer area. Biopsy samples from the gastric mucosa were taken for determination of mucosal DNA synthesis and for measurement of gastric expression of mRNA for interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha). Induction of gastric ulcers alone increased mucosal blood flow and tissue expression of mRNA for TNF-alpha and IL-1beta, whereas gastric mucosal DNA synthesis was reduced. In rats with gastric ulcers, administration of obestatin increased gastric mucosal blood flow, accelerated the healing rate of these ulcers and partly reversed the gastric ulcer-induced reduction in gastric mucosal DNA synthesis. These results were associated with a reduction in gastric mucosal expression of pro-inflammatory IL-1beta and TNF-alpha. Treatment with obestatin increases gastric mucosal blood flow and cell proliferation, leading to acceleration of healing of gastric ulcers. These effects are associated with a reduction in mucosal expression of pro-inflammatory IL-1beta and TNF-alpha.
    Medical science monitor: international medical journal of experimental and clinical research 08/2011; 17(8):BR196-200. · 1.22 Impact Factor
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    ABSTRACT: 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-1β (IL-1β) 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-1β, 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-1β 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.
    Journal of physiology and pharmacology: an official journal of the Polish Physiological Society 04/2011; 62(2):207-17. · 2.48 Impact Factor
  • Gastroenterology 01/2011; 140(5). · 12.82 Impact Factor
  • Gastroenterology 01/2011; 140(5). · 12.82 Impact Factor
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    ABSTRACT: Ghrelin is a ligand for growth hormone secretagogue receptor and stimulates release of growth hormone (GH). Recent studies have shown that treatment with ghrelin exhibits protective and therapeutic effect in the course of experimental pancreatitis. The aim of present study was to examine the role of GH and insulin-like growth factor-1 (IGF-1) in these effects. Acute pancreatitis was induced by cerulein. Study was performed on pituitary-intact hypophysectomized rats. Ghrelin was administered twice a day at the dose of 8 nmol/kg/dose. IGF-1 was given twice a day at the dose of 20 nmol/kg/dose. The severity of acute pancreatitis was assessed 0 h or 1, 2, 3, 5 and 10 days after the last dose of cerulein. Administration of cerulein led to the development of acute edematous pancreatitis. In pituitary-intact rats, treatment with ghrelin reduced biochemical indexes of the severity of acute pancreatitis and morphological signs of pancreatic damage, leading to faster regeneration of the pancreas reduction in serum concentration of pro-inflammatory interleukin-1β and decrease in serum activity of amylase and lipase. These effects were accompanied with an improvement of pancreatic blood flow and an increase in pancreatic DNA synthesis. Hypophysectomy delayed the healing of the pancreas and abolished the therapeutic effect of ghrelin. In hypophysectomized rats with pancreatitis, treatment with IGF-1 exhibits therapeutic effect similar to that observed in ghrelin-treated rats with the intact pituitary. We conclude that therapeutic effect of ghrelin in cerulein-induced pancreatitis is indirect and depends on the release of GH and IGF-1.
    Journal of physiology and pharmacology: an official journal of the Polish Physiological Society 10/2010; 61(5):599-606. · 2.48 Impact Factor
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    ABSTRACT: Recent studies have shown that pretreatment with ghrelin exhibits protective effect in the gut. Administration of ghrelin reduces gastric mucosal damage, as well as inhibits the development of experimental pancreatitis. However, this protective effect requires administration of ghrelin before gastric or pancreatic damage and thus has a limited clinical value. The aim of present study was to assess the influence of ghrelin administered after development of acute pancreatitis on the course of this disease. Acute pancreatitis was induced by cerulein. Ghrelin was administered twice a day for 1, 2, 4, 6 or 9 days at the dose of 4, 8 or 16 nmol/kg/dose. The first dose of ghrelin was given 24 hours after last injection of cerulein. The severity of acute pancreatitis was assessed between 0 h and 10 days after cessation of cerulein administration. Administration of caerulein led to the development of acute edematous pancreatitis and maximal severity of this disease was observed 24 hours after induction of pancreatitis. Treatment with ghrelin reduced morphological signs of pancreatic damage such as pancreatic edema, leukocyte infiltration and vacuolization of acinar cells, and led to earlier regeneration of the pancreas. Also biochemical indexes of the severity of acute pancreatitis, serum activity of lipase and amylase were significantly reduced in animals treated with ghrelin. These effects were accompanied by an increase in the pancreatic DNA synthesis and a decrease in serum level of pro-inflammatory interleukin-1b. Administration of ghrelin improved pancreatic blood flow in rats with acute pancreatitis. We conclude that: (1) treatment with ghrelin exhibits therapeutic effect in caerulein-induced experimental acute pancreatitis; (2) this effect is related, at least in part, to the improvement of pancreatic blood flow, reduction in proinflammatory interleukin-1beta and stimulation of pancreatic cell proliferation.
    Journal of physiology and pharmacology: an official journal of the Polish Physiological Society 08/2010; 61(4):419-27. · 2.48 Impact Factor
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    ABSTRACT: Obestatin is a peptide derived from the proghrelin, a common prohormone for ghrelin and obestatin. Obestatin, like the ghrelin has been originally extracted from rat stomach, and the stomach seems to be a major source of circulating obestatin. Previous studies have shown that administration of ghrelin exhibits protective effect in the pancreas, inhibiting the development of acute pancreatitis. Recent study has shown that obestatin promotes survival of beta-cells and pancreatic islets. Aim of the present study was to investigate the influence of obestatin administration on the development of cerulein-induced pancreatitis. Studies were performed on male Wistar rats. Acute pancreatitis was induced by cerulein given intraperitoneally 5 times at a dose of 50 microg/kg/dose with 1-h intervals. Obestatin was injected twice intraperitoneally at the dose of 4, 8 or 16 nmol/kg/dose. In control saline-treated rats, obestatin was without effect on pancreatic morphology, serum activity of pancreatic enzymes, serum level of pro-inflammatory interleukin-1beta or pancreatic cells proliferation. In animals with induction of acute pancreatitis, morphological examination showed that administration of obestatin decreased pancreatic leukocyte infiltration and vacuolization of acinar cells. These effects were accompanied by reduction in the pancreatitis-evoked increase in serum level of pancreatic digestive enzymes, lipase amylase and poly-C ribonuclease. Obestatin administered at the highest dose of 16 nmo/kg/dose reduced serum activity of these enzymes by 33, 42 and 44%, respectively. Also serum concentration of pro-inflammatory interleukin-1beta was decreased by obestatin in rats with acute pancreatitis; whereas the pancreatitis-evoked decrease in pancreatic blood flow and pancreatic DNA synthesis was partially reversed. Administration of obestatin reduces the severity of cerulein-induced acute pancreatitis. This effect is related, at least in part, to the improvement of pancreatic blood flow and reduction in proinflammatory interleukin-1beta release.
    Journal of physiology and pharmacology: an official journal of the Polish Physiological Society 09/2009; 60(3):95-101. · 2.48 Impact Factor
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    ABSTRACT: Growth hormone (GH) has been shown to protect the intestinal barrier integrity and to stimulate the production of insulin-like growth factor 1 (IGF-1), which inhibits the development of acute pancreatitis. Sensory nerves are implicated in the protection of pancreatic tissue against acute inflammation. The aim of this study was to investigate the influence of exogenous GH on acute pancreatitis (AP) and to assess the involvement of sensory nerves and IGF-1 in above effect. Studies were performed on Wistar rats. AP was induced by subcutaneous administration of caerulein (25mug/kg) to the conscious animals. GH (1 or 2mg/kg) was administered to the rats as an intraperitoneal injection 30min prior to the start of AP. To deactivate sensory nerves capsaicin was given at total dose of 100mg/kg 10days before the experiments. AP was confirmed by histological examination and manifested by the significant rises of pancreatic weight, and serum activities of lipase, TNFalpha and IL-10 (by 550%, 300% and 50%, respectively), whereas IGF-1 blood concentration was markedly reduced. Administration of GH prior to the caerulein infusion significantly increased GH, IGF-1 and IL-10 blood levels, attenuated harmful effects of AP and reduced histological manifestations of pancreatitis in the rats with intact sensory nerves. This was accompanied by the reduction of serum lipase, and TNFalpha activities. In the AP rats with capsaicin-deactivated sensory nerves GH failed to protect the pancreas against acute damage and, as a consequence of above deactivation, IGF-1 was low. CONCLUSION: GH modulates the development of acute pancreatitis in the presence of active sensory nerves probably via stimulation of IGF-1 release.
    Growth hormone & IGF research: official journal of the Growth Hormone Research Society and the International IGF Research Society 08/2009; 19(6):517-22. · 2.35 Impact Factor
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    ABSTRACT: Recent studies have shown that ghrelin exhibits gastroprotective effects. The aim of present study was to examine the influence of ghrelin administration on the healing of chronic gastric and duodenal ulcers and to evaluate the role of growth hormone (GH) and insulin-like growth factor-1 (IGF-1) in this process. In pituitary-intact or hypophysectomized rats, chronic gastric and duodenal ulcers were induced by acetic acid. After induction of ulcers, rats were treated intraperitoneally twice a day with saline, ghrelin (4, 8 or 16 nmol/kg/dose) or IGF-1 (20 nmol/kg/dose) for six or ten days. In animals with intact pituitary, treatment with ghrelin increased serum level of GH and IGF-1. These effects were accompanied by the increase in mucosal cell proliferation, mucosal blood flow and healing rate of gastric and duodenal ulcers. After hypophysectomy, the significant increase in serum level of endogenous ghrelin was observed, but the healing of gastric and duodenal ulcers was delayed. This effect was accompanied by a significant decrease in serum concentration of endogenous GH and IGF-1, and reduction in mucosal blood flow and DNA synthesis. In hypophysectomized rats, administration of exogenous ghrelin was without any effect on serum level of GH and IGF-1, healing rate of gastroduodenal ulcers or mucosal cell proliferation. In contrast to this effect, administration of IGF-1 increased mucosal cell proliferation, healing rate of gastroduodenal ulcers and mucosal blood flow in hypophysectomized rats. Conclusion: Treatment with ghrelin accelerates healing of chronic gastroduodenal ulcers and this effect is mediated by the release of endogenous GH and IGF-1.
    Journal of physiology and pharmacology: an official journal of the Polish Physiological Society 04/2009; 60(1):87-98. · 2.48 Impact Factor
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    ABSTRACT: In this review, we discuss the effects of acute and chronic exercise on appetite and food intake regulation, the potential mechanisms involved and its relationship with hormonal and metabolic changes that affect energy balance. The mechanisms of post exercise short-term appetite modification remain unclear and although the role of orexigenic and anorexigenic peptides is possible hypotheses, it still remains unproven. Motivation to eat and food intake in response to acute exercise seem to be modulated by gender, body weight and eating behavior. In general, acute exercise has no effect on subsequent El in men, whereas in women an increase in El is usually observed, either decreasing or abolishing the effects of exercise on EB. Normal weight women, unlike men, report an increased palatability of foods with exercise and do not experience the transient suppression of hunger observed immediately after exercise. The evidence to date emphasizes the need to increase physical exercise levels, particularly because of the high prevalence of obesity. More research is needed to explain the mechanisms behind the post exercise adjustments in short-term appetite control, and their long-term consequences.
    Medicina Sportiva. 01/2009; 13:82-94.
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    ABSTRACT: The initiation and progression of acute pancreatitis is associated with disturbances in pancreatic microcirculatory. Microcirculatory disorders contribute to multiorgan dysfunction syndrome in the course of acute pancreatitis. The aim of this study was to determine the influence of heparin administration on the development and the course of ischemia/reperfusion-induced pancreatitis. Methods: Acute pancreatitis was induced in rats by pancreatic ischemia followed by reperfusion. In the first series of studies, heparin was administered 0.5 h before induction of acute pancreatitis and the severity of acute pancreatitis was assessed after 6-h reperfusion. In the second series of studies, heparin was administered twice a day, starting 24 h after the initiation of reperfusion. In both series of studies, heparin was administered subcutaneously at the dose of 150 U/kg. Results: Treatment with heparin, before induction of pancreatitis, inhibits the development of morphological signs of acute pancreatitis and reduced the pancreatitis-evoked increase in plasma level of pancreatic enzymes and pro-inflammatory interleukin-1beta. These effects have been accompanied with improvement of pancreatic blood flow, pancreatic DNA synthesis and reduction in plasma concentration of D-dimer. Administration of heparin after induction of acute pancreatitis accelerates normalization of pancreatic histology, and reduces biochemical markers of the severity of acute pancreatitis. These effects have been accompanied with the improvement of pancreatic circulation, increase in APTT and reduction in plasma D-dimer level. Conclusions: Treatment with heparin inhibits the development of ischemia/reperfusion-induced pancreatitis and accelerates pancreatic regeneration in the course of this disease.
    Journal of physiology and pharmacology: an official journal of the Polish Physiological Society 10/2008; 59 Suppl 4:103-25. · 2.48 Impact Factor
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    ABSTRACT: Some recent studies indicate that cannabis may induce acute pancreatitis in humans and administration of anandamide increases the severity of acute pancreatitis; whereas another study exhibits some therapeutic effects in acute pancreatitis. Aim of the present study was to discover what is the reason for these opposite confusing results and to determine the role of sensory nerves in this effect. Acute pancreatitis was induced in rats by cerulein. Anandamide, an endogenous cannabinoid, was administered i.p. (1.5 micromol/kg) before or 2 h after cerulein administration. Stimulation of sensory nerves was performed by capsaicin (0.5 mg/kg s.c.). In rats treated with combination of anandamide plus capsaicin, capsaicin was given 10 min after each dose of anandamide. After the last injection of cerulein or 4 h later, the study was terminated. In our study we observed that stimulation of sensory nerves by capsaicin, before administration of cerulein, reduced the severity of acute pancreatitis. Anandamide, administered alone before cerulein, increased pancreatic damage in acute pancreatitis. Anandamide administered in combination with capsaicin, before cerulein, abolished the capsaicin-induced protective effect on the pancreas. Opposite effects were observed when capsaicin and anandamide were administered after injection of cerulein. Capsaicin increased the severity of acute pancreatitis, whereas anandamide reduced pancreatic damage and reversed the deleterious effect of capsaicin. We conclude that the effect of anandamide on the severity of acute pancreatitis depends on the phase of this disease. Administration of anandamide, before induction of pancreatitis, aggravates pancreatic damage; whereas anandamide administered after induction of pancreatitis, reduces the severity of acute pancreatitis. Sensory nerves are involved in the mechanism of this biphasic effect of anandamide.
    European Journal of Pharmacology 07/2008; 591(1-3):284-92. · 2.59 Impact Factor

Publication Stats

2k Citations
685.96 Total Impact Points

Institutions

  • 1995–2013
    • Jagiellonian University
      • Department of Physiology
      Cracovia, Lesser Poland Voivodeship, Poland
  • 2009
    • Akademickie Centrum Komputerowe CYFRONET AGH
      Cracovia, Lesser Poland Voivodeship, Poland
  • 1976–2005
    • Friedrich-Alexander Universität Erlangen-Nürnberg
      • • Department of Experimental and Clinical Pharmacology and Toxicology
      • • Institute of Physics
      Erlangen, Bavaria, Germany
  • 1996–2004
    • Collegium Medicum of the Jagiellonian University
      Cracovia, Lesser Poland Voivodeship, Poland
  • 1993–1998
    • University of Münster
      • Faculty of Medicine
      Münster, North Rhine-Westphalia, Germany
    • Krakow University Hospital
      Cracovia, Lesser Poland Voivodeship, Poland