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| 1 | 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 |
| 2 | Mathematical Modeling of Rate-independent Pseudoelastic SMA Material显示文摘 | Wieslaw G Andrzej W Artur Z | | 0，，： | 1 |
| 3 | Crystallization of gahnite in CMAS glass forming system - mechanism and process kinetics 显示文摘 | DANIELA H TOMASZ O WIESLAW W | 2010 | Adv Sci Tech2010，68，： | 1 |
| 4 | Synthesis and spectral properties of colloidal Nd3 - doped NaYF4 nanocrystals 显示文摘 | Artur B Dominika W Marcin N Wieslaw S | 2011 | Optical Materials2011，33，： | 1 |
| 5 | Preparation and Properties of Flocculants Derived from Polystyrene Waste显示文摘 | AGNIESZKA WOLINSKA BARBARA SZOLTYSIK | 2005 | Polymer Degradation and Stability2005，90，： | 1 |
| 6 | Non-proportionality and energy resolution of CsI(T1)显示文摘 | AGNIESZKA S EUKASZS W WIESLAW C | 2007 | IEEE Transactions on Nuclear Science2007，54，5： | 1 |
| 7 | Liquid state machine built of Hodgkin-Huxley neurons and pattern recognition显示文摘 | GRZEGORZ M W WIESLAW A K | 2004 | Neurocomputing2004，5860，： | 1 |
| 8 | Separation of individual catechins from green tea using silica gel column chromatography and HPLC显示文摘 | RYSZARD A FEREIDOON S WIESLAW W | 2003 | Journal of Food Lipids2003，10，2： | 1 |
| 9 | A new Java-based software environment for distributed measurement systems designing显示文摘 | MICHAL K WIESLAW W | 2001 | Instrumentation and Measurement Technology2001，，1： | 1 |
| 10 | Grapefruit-seed extract attenuates ethanol-and stress-induced gastric lesions via activation of prostaglandin, nitric oxide and sensory nerve pathways显示文摘AIM: Grapefruit-seed extract (GSE) containing flavonoids, possesses antibacterial and antioxidative properties but whether it influences the gastric defense mechanism and gastroprotection against ethanol- and stress-induced gastric lesions remains unknown. METHODS: We compared the effects of GSE on gastric mucosal lesions induced in rats by topical application of 100% ethanol or 3.5 h of water immersion and restraint stress (WRS) with or without (A) inhibition of cyclooxygenase (COX)-1 activity by indomethacin and rofecoxib, the selective COX-2 inhibitor, (B) suppression of NO-synthase with L-NNA (20 mg/kg ip), and (C) inactivation by capsaicin (125 mg/kg sc) of sensory nerves with or without intragastric (ig) pretreatment with GSE applied 30 min prior to ethanol or WRS. One hour after ethanol and 3.5 h after the end of WRS, the number and area of gastric lesions were measured by planimetry, the gastric blood flow (GBF) was assessed by H2-gas clearance technique and plasma gastrin levels and the gastric mucosal generation of PGE2, superoxide dismutase (SOD) activity and malonyldialdehyde (MDA) concentration, as an index of lipid peroxidation were determined. RESULTS: Ethanol and WRS caused gastric lesions accompanied by the significant fall in the GBF and SOD activity and the rise in the mucosal MDA content. Pretreatment with GSE (8-64 mg/kg i g) dose-dependently attenuated gastric lesions induced by 100% ethanol and WRS; the dose reducing these lesions by 50% (ID50) was 25 and 36 mg/kg, respectively, and this protective effect was similar to that obtained with methyl PGE2 analog (5 μg/kg i g). GSE significantly raised the GBF, mucosal generation of PGE2, SOD activity and plasma gastrin levels while attenuating MDA content. Inhibition of PGE2 generation with indomethacin or rofecoxib and suppression of NO synthase by L-NNA or capsaicin denervation reversed the GSE-induced protection and the accompanying hyperemia. Co-treatment of exogenous calcitonine gene-related peptide (CGRP) with GSE restored the protection and accompanying hyperemic effects of GSE in rats with capsaicin denervation. CONCLUSION: GSE exerts a potent gastroprotective activity against ethanol and WRS-induced gastric lesions via an increase in endogenous PG generation, suppression of lipid peroxidation and hyperemia possibly mediated by NO and CGRP released from sensory nerves. | Tomasz Brzozowski Peter C Konturek Danuta Drozdowicz Stanislaw J Konturek Oxana Zayachivska Robert Pajdo Slawomir Kwiecien Wieslaw W Pawlik Eckhart G Hahn | 2005 | World Journal of Gastroenterology2005，11，41： | 1 |
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