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Am J Physiol Gastrointest Liver Physiol 278: G839-G846, 2000;
0193-1857/00 $5.00
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Vol. 278, Issue 6, G839-G846, June 2000

Resistance to apoptosis is a mechanism of adaptation of rat stomach to aspirin

Barbara M. Alderman, Gregory A. Cook, Mary Familari, Neville D. Yeomans, and Andrew S. Giraud

University of Melbourne, Department of Medicine, Western Hospital, Footscray, Victoria 3011, Australia

Adaptation of the gastric mucosa to nonsteroidal anti-inflammatory drug-induced injury is a well-documented phenomenon, but the mechanisms are not known. We investigated whether changes in stress protein expression and apoptosis play roles in adaptation of rat stomach to aspirin. RT-PCR and Western blotting techniques were used to analyze mRNA and protein expression of HSP72 and HSP90 and cleavage of caspase 3 protein. Apoptosis was detected by the TUNEL method and quantified. HSP72 mRNA and protein expression was unchanged in adapted mucosa, whereas HSP90 mRNA and protein levels decreased. Caspase 3 protein was activated, and the number of apoptotic cells increased in mucosa after one aspirin dose. However, in adapted mucosa after aspirin, activated caspase 3 and the number of apoptotic cells had returned to basal levels. Induction of the stress response was found not to be a mechanism of mucosal adaptation against multiple doses of aspirin. Our results lead us to propose instead that resistance to aspirin-induced apoptosis plays a role in the protective phenomenon of adaptation.

stress proteins; caspase 3; nonsteroidal anti-inflammatory drugs; gastric mucosa


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