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Therapeutic proteasome inhibition in experimental acute pancreatitis

World journal of Gastroenterology 2007年第33期13卷 4452-4457页

作者： Tamás Letoha Liliána Z Fehér László Pecze Csaba Somlai Ilona Varga józsef kaszaki Gábor Tóth Csaba Vizler László Tiszlavicz Tamás Takács Department of Medical Chemistry University of Szeged H-6720 Szeged Hungary Institute of Biochemistry Biological Research Center of the HungarianAcademy of Sciences H-6726 Szeged Hungary Department of Genetics and Molecular Biology University of Szeged H-6726 Szeged Hungary Institute of Surgical Research University of Szeged H-6720 Szeged Hungary Department of Pathology University of Szeged H-6720 Szeged Hungary First Department of Medicine University of Szeged H-6720 Szeged Hungary

AIM： To establish the therapeutic potential of proteasome inhibition, we examined the therapeutic effects of MG132 （Z-Leu-Leu-Leu-aldehyde） in an experimental model of acute pancreatitis. METHODS： Pancreatitis was induced in rats by two hourly intraperitoneal （ip） injections of cholecystokinin octapeptide （CCK; 2×100μg/kg） and the proteasome inhibitor MG132 （10 mg/kg ip） was administered 30 min after the second CCK injection. Animals were sacrificed 4 h after the first injection of CCK. RESULTS： Administering the proteasome inhibitor MG132 （at a dose of 10 mg/kg, ip） 90 min after the onset of pancreatic inflammation induced the expression of cell-protective 72 kDa heat shock protein （HSP72） and decreased DNA-binding of nuclear factor-κB （NF-κB）. Furthermore MG132 treatment resulted in milder inflammatory response and cellular damage, as revealed by improved laboratory and histological parameters of pancreatitis and associated oxidative stress. CONCLUSION： Our findings suggest that proteasome inhibition might be beneficial not only for the prevention, but also for the therapy of acute pancreatitis.

关键词： Acute pancreatitis Cholecystokinin octapeptide Proteasome inhibition Nuclear factor-κB Heat shock proteins

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A nuclear import inhibitory peptide ameliorates the severity of cholecystokinin-induced acute pancreatitis

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World journal of Gastroenterology 2005年第7期11卷 990-999页

作者： Tamás Letoha Csaba Somlai Tamáas Takács Annamária Szabolcs Katalin jármay Zoltán Rakonczay jr Péter Hegyi Ilona Varga józsef kaszaki István Krizbai Imre Boros Ern(?) Duda Erzsébet Kusz Botond Penke Department of Medical Chemistry First Department of Medicine Department of Genetics and Molecular Biology Institute of Surgical Research Institute of Biophysics Institute of Biochemistry

AIM: To assess the effect of our novel cell-permeable nuclear factor-kappaB (NF-κB) inhibitor peptide PN50 in an experimental model of acute pancreatitis. PN50 was produced by conjugating the cell-penetrating penetratin peptide with the nuclear localization signal of the NF-κB p50 ***: Pancreatitis was induced in male Wistar rats by administering 2×100 μg/kg body weight of cholecystokininoctapeptide (CCK) intraperitoneally (IP) at an interval of 1 h. PN50-treated animals received 1 mg/kg of PN50 IP 30 min before or after the CCK injections. The animals were sacrificed 4 h after the first injection of ***: All the examined laboratory (the pancreatic weight/body weight ratio, serum amylase activity,pancreatic levels of TNF-α and IL-6, degree of lipid peroxidation, reduced glutathione levels, NF-κB binding activity, pancreatic and lung myeloperoxidase activity) and morphological parameters of the disease were improved before and after treatment with the PN50 *** to the histological findings, PN50 protected the animals against acute pancreatitis by favoring the induction of apoptotic, as opposed to necrotic acinar cell death associated with severe acute ***: Our study implies that reversible inhibitors of stress-responsive transcription factors like NF-κB might be clinically useful for the suppression of the severity of acute pancreatitis.

关键词： Acute pancreatitis Peptide delivery Penetratin NF-κB inhibition

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Systemic phosphatidylcholine pretreatment protects canine esophageal mucosa during acute experimental biliary reflux

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World journal of Gastroenterology 2006年第2期12卷 271-279页

作者： Gabor Eros jozsef kaszaki Miklos Czobel Mihaly Boros Institute of Surgical Research University of SzegedHungary

AIM： To characterize the consequences of short-term exposure to luminal bile on mucosal mast cell reactions in a canine model, and to determine the effects of systemic phosphatidylcholine pretreatment in this condition. METHODS： Twenty mongrel dogs were used for experiments. Group 1 （n =5） served as a salinetreated control, while in group 2 （n = 5） the esophagus was exposed to bile for 3 h. In group 3 （n =5） the animals were pretreated with 7-nitroindazole to inhibit the neuronal isoform of nitric oxide synthase. In group 4 （n = 5） phosphatidylcholine solution （50 rng/kg） was administered iv before the biliary challenge. Mucosal microcirculation was observed by intravital videomicroscopy. Myeloperoxidase and nitric oxide synthase activities, the degrees of mast cell degranulation and mucosal damage were evaluated via tissue biopsies. RESULTS： Exposure to bile evoked significant mast cell degranulation and leukocyte accumulation. The red blood cell velocity and the diameter of the postcapillary venules increased significantly. The tissue ATP content and constitutive nitric oxide synthase activity decreased, while the inducible nitric oxide synthase activity increased significantly as compared to the control values. 7-nitroindazole treatment significantly exacerbated the mucosal mast cell degranulation and tissue damage. Tn contrast, phosphatidylcholine pretreatment prevented the bile-induced ATP depletion, the inducible nitric oxide synthase and myeloperoxidase activity and the mast cell degranulation increased. CONCLUSION： The neuronal nitric oxide synthasemast cell axis plays an important role in the esophageal mucosal defense system. Systemic phosphatidylcholine pretreatment affords effective protection through ameliorating the bile-induced ATP depletion and secondary inflammatory reaction.

关键词： Esophagus Bile Neuronal nitric oxide Mast cell Microcirculation Inflammation

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Effect of melatonin on the severity of L-arginine-induced experimental acute pancreatitis in rats

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World journal of Gastroenterology 2006年第2期12卷 251-258页

作者： Annamaria Szabolcs Russel j Reiter Tamas Letoha Peter Hegyi Gabor Papai Ilona Varga Katalin jarmay jozsef kaszaki Reka Sari Zoltan Rakonczay jr janos Lonovics Tamas Takacs st Department of Medicine University of SzegedHungary Department of Cellular and Structural Biology University of TexasHealth Science CentreSan AntonioTexasUnited States Institute of Chemistry University of SzegedHungary Biological Research Centre Hungarian Academy of SciencesSzegedHungary Biological Isotope Laboratory University of SzegedHungary Institute of Experimental Surgery University of SzegedHungary

AIM： To determine the effect of melatonin pre- and post-treatment on the severity of L-arginine （L-Arg） -induced experimental pancreatitis in rats. METHODS： Male Wistar rats （25） were divided into five groups. Those in group A received two injections of 3.2 g/kg body weight L-Arg i.p. at an interval of 1 h. In group MA, the rats were treated with 50 mg/kg body weight melatonin i.p. 30 min prior to L-Arg administration. In group AM, the rats received the same dose of melatonin 1 h after L-Arg was given. In group M, a single dose of melatonin was administered as described previously. In group C the control animals received physiological saline injections i.p. All rats were exsanguinated 24 h after the second L-Arg injection. RESULTS： L-Arg administration caused severe necrotizing pancreatitis confirmed by the significant elevations in the serum amylase level, the pancreatic weight/body weight ratio （pw/bw）, the pancreatic IL-6 content and the myeloperoxidase activity, relative to the control values. Elevation of the serum amylase level was significantly reduced in rats given melatonin following L-Arg compared to rats injected with L-Arg only. The activities of the pancreatic antioxidant enzymes （Cu/Zn-superoxide dismutase （CulZn-SOD） and catalase （CAT）） were significantly increased 24 h after pancreatitis induction. Melatonin given in advance of L-Arg significantly reduced the pancreatic CAT activity relative to that in the rats treated with L-Arg alone. In the liver, L-Arg significantly increased the lipid peroxidation level, and the glutathione peroxidase and Cu/Zn-SOD activities, whereas the Mn-SOD activity was reduced as compared to the control rats. Melatonin pre-treatment prevented these changes. CONCLUSION： Melatonin is an antioxidant that is able to counteract some of the L-Arg-induced changes during acute pancreatitis, and may therefore be helpful in the supportive therapy of patients with acute necrotizing pancreatitis.

关键词： Acute pancreatitis Melatonin Scavengers

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