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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Fornai, Matteo Colucci, Rocchina Antonioli, Luca Awwad, Oriana Ugolini, Clara Tuccori, Marco Fulceri, Federica Natale, Gianfranco Basolo, Fulvio Blandizzi, Corrado |
| Description | Country affiliation: Italy Author Affiliation: Fornai M ( Interdepartmental Centre for Research in Clinical Pharmacology and Experimental Therapeutics, University of Pisa, Via Roma 55, 56126 Pisa, Italy.) |
| Abstract | Proton pump inhibitors promote ulcer repair in nonsteroidal anti-inflammatory drug (NSAID)-treated patients with ongoing NSAID-induced gastric toxicity, although the underlying mechanisms remain unclear. We examined the healing mechanisms of esomeprazole on NSAID-induced gastric ulcerations in the presence of a continued NSAID treatment. Ulcerations were induced in rats by oral indomethacin (6µmol/kg/day) for 14 days. Indomethacin administration was continued, alone or combined with equivalent acid inhibitory doses of esomeprazole (5µmol/kg/day), lansoprazole (15µmol/kg/day) or famotidine (20µmol/kg/day), for additional 7 days. Stomachs were then processed for: histomorphometric analysis of mucosal injury; mucosal levels of prostaglandin E(2) (PGE(2)) and malondialdehyde (MDA); expression of vascular endothelial growth factor (VEGF), proliferating cell nuclear antigen (PCNA), caspase-3, and cyclooxygenase-2 (COX-2) (Western blot); expression of Ki-67 (immunohistochemistry). Indomethacin for 14 days elicited mucosal damage, reduced PGE(2) levels and increased MDA. After additional 7 days, indomethacin induced the following effects: further enhancement of mucosal damage and MDA content; decrease in PGE(2) levels; increase in COX-2 and activated caspase-3 expression; decrease in VEGF, PCNA and Ki-67 expression. In the presence of indomethacin, esomeprazole and lansoprazole were more effective than famotidine in promoting resolution of mucosal damage. Concomitantly, esomeprazole and lansoprazole, but not famotidine, restored PCNA and Ki-67 expression, and normalized MDA levels. Moreover, esomeprazole, lansoprazole and famotidine partly counteracted caspase-3 activation, without affecting VEGF expression. The healing activity of esomeprazole on indomethacin-induced gastric ulcerations can be ascribed to two mechanisms: (1) acid-dependent reduction of pro-apoptotic signalling; (2) acid-independent restoration of proliferating/repairing pathways. |
| File Format | HTM / HTML |
| ISSN | 10436618 |
| Issue Number | 1 |
| Volume Number | 63 |
| Journal | Pharmacological Research |
| e-ISSN | 10961186 |
| Language | English |
| Publisher | Elsevier |
| Publisher Date | 2011-01-01 |
| Publisher Place | Netherlands |
| Access Restriction | One Nation One Subscription (ONOS) |
| Subject Keyword | Discipline Pharmacology Anti-ulcer Agents Pharmacology Esomeprazole Gastric Mucosa Drug Effects Indomethacin Proton Pump Inhibitors Stomach Ulcer Drug Therapy Wound Healing 2-pyridinylmethylsulfinylbenzimidazoles Animals Anti-inflammatory Agents, Non-steroidal Apoptosis Blotting, Western Caspase 3 Metabolism Cell Proliferation Cyclooxygenase 2 Dinoprostone Disease Models, Animal Famotidine Gastric Acid Secretion Pathology Histamine H2 Antagonists Immunohistochemistry Ki-67 Antigen Lansoprazole Male Malondialdehyde Proliferating Cell Nuclear Antigen Rats Rats, Wistar Chemically Induced Time Factors Vascular Endothelial Growth Factor A Comparative Study Journal Article |
| Content Type | Text |
| Resource Type | Article |
| Subject | Pharmacology |
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