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| 1 | Hormonal protection in acute pancreatitis by ghrelin, leptin and melatonin显示文摘Acute pancreatitis is a nonbacterial disease of the pancreas.The severe form of this ailment is characterized by high mortality.Whether acute pancreatitis develops as the severe type or resolves depends on the intensity of the inflammatory process which is counteracted by the recruitment of innate defense mechanisms.It has been shown that the hormones ghrelin,leptin and melatonin are able to modulate the immune function of the organism and to protect the pancreas against inflammatory damage.Experimental studies have demonstrated that the application of these substances prior to the induction of acute pancreatitis significantly attenuated the intensity of the inflammation and reduced pancreatic tissue damage.The pancreatic protective mechanisms of the above hormones have been related to the mobilization of non-specific immune defense,to the inhibition of nuclear factor kappa B and modulation of cytokine production,to the stimulation of heat shock proteins and changes of apoptotic processes in the acinar cells,as well as to the activation of antioxidant system of the pancreatic tissue.The protective effect ofghrelin seems to be indirect and perhaps dependent on the release of growth hormone and insulin-like growth factor 1.Leptin and ghrelin,but not melatonin,employ sensory nerves in their beneficial action on acute pancreatitis.It is very likely that ghrelin,leptin and melatonin could be implicated in the natural protection of the pancreatic gland against inflammatory damage because the blood levels of these substances increase in the initial phase of pancreatic inflammation.The above hormones could be a part of the innate resistance system which might remove noxious factors and could suppress or attenuate the inflammatory process in the pancreas. | Jolanta Jaworek Stanis?aw Jan Konturek | 2014 | World Journal of Gastroenterology2014，20，45： | 10 |
| 2 | Helicobacter pylori upregulates prion protein expression in gastric mucosa: A possible link to prion disease显示文摘AIM: Pathological prion protein (PrPSC) is responsible for the development of transmissible spongiform encephalopathies (TSE). While PrPc enters the organism via the oral route, less data is available to know about its uptake and the role of gastrointestinal inflammation on the expression of prion precursor PrPc, which is constitutively expressed in the gastric mucosa.METHODS: We studied PrPc expression in the gastric mucosa of 10 Helicobacter pylori-positive patients before and after successful H pylori eradication compared to non-infected controls using RT-PCR and Western blotting.The effect of central mediators of gastric inflammation,i.e., gastrin, prostaglandin E2 (PGE2), tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β) on PrPc expression was analyzed in gastric cell lines.RESULTS: PrPc expression was increased in H pyloriinfection compared with non-infected controls and decreased to normal after successful eradication. Gastrin,PGE2, and IL-1β dose-dependently upregulated PrPc in gastric cells, while TNF-α had no effect.CONCLUSION: H pylori infection leads to the upregulation of gastric PrPc expression. This can be linked to H pylori induced hypergastrinemia and increased mucosal PGE2 and IL-1β synthesis.H pylori creates a milieu for enhanced propagation of prions in the gastrointestinal tract. | Peter C Konturek Karolina Bazela Vitally Kukharskyy Michael Bauer Eckhart G Hahn Detlef Schuppan | 2005 | World Journal of Gastroenterology2005，11，48： | 9 |
| 3 | Pioglitazone, a specific ligand of peroxisome proliferator-activated receptor-gamma, protects pancreas against acute cerulein-induced pancreatitis显示文摘ABM: To determine the effect of pioglitazone, a specific peroxisome proliferator-activated receptor-γ(PPARγ) ligand, on the development of acute pancreatitis (AP) and on the expression of heat shock protein 70 (HSP70) in the pancreas. METHODS: AP was induced in rats by subcutaneous infusion of cerulein for 5 h. Pancreatic blood flow was measured by laser Doppler flowmetry. Plasma lipase activity, interleukin-1β (IL-1β) and IL-10 were determined, Pancreatic weight and histology were evaluated and pancreatic DNA synthesis and blood flow as well as pancreatic mRNA for IL-1β and HSP70 were assessed in rats treated with pioglitazone alone or in combination with cerulein. RESULTS: Pioglitazone administered (10-100 mg/kg i.g.) 30 min before cerulein, attenuated dose-dependently the pancreatic tissue damage in cerulein-induced pancreatitis (CIP) as demonstrated by the improvement of pancreatic histology, reduction in plasma lipase activity, plasma concentration of pro-inflammatory IL-1β and its gene expression in the pancreas and attenuation of the pancreatitis-evoked fall in pancreatic blood flow. CIP increased pancreatic HSP70 mRNA and protein expression in the pancreas and this effect was enhanced by pioglitazone treatment. CONCLUSION: Pioglitazone attenuates CIP and the beneficial effect of this pioglitazone is multifactorial probably due to its anti-inflammatory activities, to the suppression of IL-1β and to the over-expression of HSP70. PPARγ ligands could represent a new therapeutic option in the treatment of AP. | Peter C Konturek Artur Dembinski Zygmunt Warzecha Grzegorz Burnat Piotr Ceranowicz Eckhart G Hahn Marcin Dembinski Romana Tomaszewska Stanislaw J Konturek | 2005 | World Journal of Gastroenterology2005，11，40： | 7 |
| 4 | Ghrelin and gastrin in advanced gastric cancer before and after gastrectomy显示文摘AIM: To investigate plasma ghrelin, gastrin and growth hormone secretagogue receptor (GHS-R) expression in advanced gastric cancer (GC) before and after resection. METHODS: Seventy subjects in whom endoscopy of the upper gastrointestinal tract was performed in the Department of General Surgery at Cracow University during the past decade: (1) 25 patients with GC associated with Helicobacter pylori (H. pylori) infection; (2) 10 patients with GC 4-5 years after (total or subtotal) gastrectomy; (3) 25 healthy H. pylori-negative controls, matched by age and BMI to the above two groups; and (4) 10 GC patients 4-5 years after total gastrectomy. Ghrelin and gastrin plasma concentrations were measured by specific radioimmunoassay under fasting conditions and postprandially at 60 and 90 min after ingestion of a mixed meal. GHS-R expression was examined in biopsy samples from intact healthy mucosa and GC tissue using semi-quantitative reverse transcription-polymerase chain reaction. RESULTS: In healthy controls, fasting plasma ghrelin levels were significantly elevated and declined markedly at 60 and 90 min after a mixed meal. The concomitant enhanced ghrelin, GHS-R and gastrin expression in GC tissue over that recorded in intact mucosa, and the marked rise in plasma gastrin in these subjects under fasting conditions indicate the role of these hormonal factors in GC formation. Fasting plasma levels and postprandial response of ghrelin and gastrin appear to be inversely correlated in healthy subjects. Feeding in the controls resulted in a significant fall in plasma ghrelin with a subsequent rise in plasma gastrin, but in H. pylori-positive GC patients submitted to total or distal gastrectomy, feeding failed to affect significantly the fall in plasma ghrelin that was recorded in these patients before surgery. Fasting ghrelin concentrations were significantly lower in patients 4-5 years after total gastrectomy compared to those in healthy controls and to these in GC patients before surgery. CONCLUSION: Elevated plasma gastrin and suppression of fasting ghrelin in patients with GC suggest the existence of a close relationship between these two hormones in gastric carcinogenesis. | Anna Zub-Pokrowiecka Kazimierz Rembiasz Peter C Konturek Andrzej Budzyński Stanisaw J Konturek Marek Winiarski Wadysaw Bielański | 2011 | World Journal of Gastroenterology2011，17，4： | 7 |
| 5 | Ischemic preconditioning inhibits development of edematous cerulein-induced pancreatitis: Involvement of cyclooxygenases and heat shock protein 70显示文摘AIM: To determine whether ischemic preconditioning (IP)affects the development of edematous cerulein-induced pancreatitis and to assess the role of cyclooxygenase-1 (COX-1), COX-2, and heat shock protein 70 (HSP 70) in this process.METHODS: In male Wistar rats, IP was performed by damping of celiac artery (twice for 5 min at 5-min intervals).Thirty minutes after IP or sham operation, acute pancreatitis was induced by cerulein. Activity of COX-1 or COX-2 was inhibited by resveratrol or rofecoxib, respectively (10 mg/kg).RESULTS: IP significantly reduced pancreatic damage in cerulein-induced pancreatitis as demonstrated by the improvement of pancreas histology, reduction in serum lipase and poly-C ribonuclease activity, and serum concentration of pro-inflammatory interleukin (IL)-1β.Also, IP attenuated the pancreatitis-evoked fall in pancreatic blood flow and pancreatic DNA synthesis.Serum level of anti-inflammatory IL-10 was not affected by IP. Cerulein-induced pancreatitis and IP increased the content of HSP 70 in the pancreas. Maximal increase in HSP 70 was observed when IP was combined with cerulein-induced pancreatitis. Inhibition of COXs, especially COX-2, reduced the protective effect of IP in edematous pancreatitis.CONCLUSION: Our results indicate that IP reduces pancreatic damage in cerulein-induced pancreatitis and this effect, at least in part, depends on the activity of COXs and pancreatic production of HSP 70. | Zygmunt Warzecha Artur Dembinski Piotr Ceranowicz Stanislaw J Konturek Marcin Dembinski Wieslaw W Pawlik Romana Tomaszewska Jerzy Stachura Beata Kusnierz-Cabala Jerzy W Naskalski Peter C Konturek | 2005 | World Journal of Gastroenterology2005，11，38： | 2 |
| 6 | Effect of Adiponectin and Ghrelin on Apoptosis of Barrett Adenocarcinoma Cell Line显示文摘 | Peter C. Konturek Grzegorz Burnat Tilman Rau Eckhart G. Hahn Stanislaw Konturek | 2008 | Digestive Diseases and Sciences2008，，3： | 2 |
| 7 | Expression of epidermal growth factor-alpha after exposure of rat gastric mucosa to stress显示文摘 | Emst H Brzozowski T | 1996 | Scand J Gastroenterol1996，31，3： | 1 |
| 8 | Epidermal growth and transforming growth factor alpha:Role in protection and healing of gastric mucosal lesions显示文摘 | Konturek PC Konturek Sj Brzozowski T | 1995 | Eur J Gast roenterol Hepatol1995，7，10： | 1 |
| 9 | Role of salivary glands and epidermal growth factor (EGF) in gastric secretion and mucosal integrity in rats exposed to stress显示文摘 | Konturek S J Brzozowski T Konturek P K | 1991 | Regul Peptides1991，32，： | 1 |
| 10 | Five-year Follow-up of a Randomized Clinical Trial of Total Thyroidectomy versus Dunhill Operation versus Bilateral Subtotal Thyroidectomy for Multinodular Nontoxic Goiter显示文摘 | Marcin Barczyński Aleksander Konturek Alicja Hubalewska-Dydejczyk Filip Go?kowski Stanis?aw Cichoń Wojciech Nowak | 2010 | World Journal of Surgery2010，，6： | 1 |
| 11 | Postprandial response of ghrelin and PYY and indices of low-grade chronic inflam- mation in lean young women with polyeystic ovary syndrome显示文摘 | Zwirska-Korezala K Sodowski K Konturek SJ etal | 2008 | l Physiol Pharmacol2008，59，2： | 1 |
| 12 | Role of cholecystokinin in the control of gastric emptying and secretory response to a fatty meal in normal subjects and duodenal ulcer patients显示文摘 | Konturek JW Thor P Maczka M | 1994 | Scand J Gastroenterol1994，29，7： | 1 |
| 13 | Role of gastric acidecretion in progression of acute gastric erosions induced by ischemiarepeffusion into gastric ulcers 显示文摘 | Brzozowski T Konturek PC Konturek S J | 2000 | Eur Pharmacol2000，398，1： | 1 |
| 14 | The efficacy of hydrotalcite compared with OTC famotidine in the ondemand treatment of gastroesophageal reflux disease:a non-infefioritytrial显示文摘 | Konturek JW Beneke M Koppermann R | 2007 | Med Sci Monit2007，13，1： | 1 |
| 15 | Influence of COX-2 inhibition by rofecoxib on serum and tumor progastrin and gastrin levels and expression of PPAG gamma and apoptosis-related proteins in gastric cancer patients显示文摘 | Konturek PC Konturek SJ Bidanski W | 2003 | Dig Dis Sci2003，48，10： | 1 |
| 16 | Expression of survivin and caspase 3 in gastric cancer显示文摘 | KAMA J KONTUREK S J MARLICZ K | 2003 | Disge Dise and Sci2003，48，2： | 1 |
| 17 | Role of brain-gut axis in healing of gastric ulcers 显示文摘 | Konturek P C Brzozowski B Burnat G | 2004 | J Physiol Pharmacol2004，55，1： | 1 |
| 18 | Helicobacter pylori infection in coronary artery disease 显示文摘 | Kowalski M Pawlik M Konturek JW | 2006 | J Physiol Pharmacol2006，9，3： | 1 |
| 19 | Role of prostaglandins in gastroprotection and gastric adaptation 显示文摘 | Brzozowski T Konturek PC Konturek SJ | 2005 | J Physiol Pharmacol2005，565，： | 1 |
| 20 | Expression of sur-vivin and caspase-3in gastric cancer显示文摘 | Kania J Konturek SJ Marlicz K | 2003 | Dig Dis Sci2003，48，2： | 1 |
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