| Autor: |
Ricci V; Institute of Human Physiology, University of Pavia, 27100 Pavia, Italy. ricci@chifis.unipv.it, Manzo BA, Tuccillo C, Boquet P, Ventura U, Romano M, Zarrilli R |
| Jazyk: |
angličtina |
| Zdroj: |
American journal of physiology. Gastrointestinal and liver physiology [Am J Physiol Gastrointest Liver Physiol] 2002 Sep; Vol. 283 (3), pp. G511-20. |
| DOI: |
10.1152/ajpgi.00046.2002 |
| Abstrakt: |
The relationship between nonsteroidal anti-inflammatory drugs (NSAIDs) and Helicobacter pylori-induced gastric mucosal injury is still under debate. VacA toxin is an important H. pylori virulence factor that causes cytoplasmic vacuolation in cultured cells. Whether and how NSAIDs affect VacA-induced cytotoxicity is unclear. This study was designed to evaluate the effect of NSAIDs on H. pylori VacA toxin-induced cell vacuolation in human gastric mucosal cells in culture (MKN 28 cell line). Our data show that 1) NSAIDs (indomethacin, aspirin, and NS-398) inhibit VacA-induced cell vacuolation independently of inhibition of cell proliferation and prostaglandin synthesis; 2) NSAIDs impair vacuole development/maintenance without affecting cell binding and internalization of VacA; and 3) NSAIDs, as well as the chloride channel blocker 5-nitro-2-(3-phenylpropylamino) benzoic acid, also inhibit cell vacuolation induced by ammonia. We thus hypothesize that NSAIDs might protect MKN 28 cells against VacA-induced cytotoxicity by inhibiting VacA channel activity required for vacuole genesis. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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