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Am J Physiol Gastrointest Liver Physiol 281: G1092-G1100, 2001;
0193-1857/01 $5.00
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Vol. 281, Issue 4, G1092-G1100, October 2001

NSAIDs induce both necrosis and apoptosis in guinea pig gastric mucosal cells in primary culture

Wataru Tomisato1, Shinji Tsutsumi1, Kazuhito Rokutan2, Tomofusa Tsuchiya1, and Tohru Mizushima1,3

1 Faculty of Pharmaceutical Sciences, Okayama University and 3 Precursory Research for Embryonic Science and Technology, Japan Science and Technology Corporation, Okayama 700-8530; and 2 Department of Nutrition, School of Medicine, University of Tokushima, Tokushima 770-8503, Japan

A major clinical problem encountered with the use of nonsteroidal anti-inflammatory drugs (NSAIDs) such as indomethacin is gastropathy. In this study, we examined, using guinea pig gastric mucosal cells in primary culture, how NSAIDs damage gastric mucosal cells. The short-term treatment of cells with high concentrations of indomethacin decreased cell viability in the absence of apoptotic DNA fragmentation, chromatin condensation, or caspase activation. Cells lost membrane integrity with this short-term indomethacin treatment, suggesting that indomethacin induced necrosis under these conditions. In contrast, the long-term treatment of cells with low concentrations of indomethacin decreased cell viability and was accompanied by apoptotic DNA fragmentation, chromatin condensation, and caspase activation. Pretreatment of cells with inhibitors of caspases or protein synthesis suppressed cell death caused by long-term indomethacin treatment, suggesting that apoptosis was induced when the inhibitors were not present. These results imply that NSAIDs cause gastric mucosal damage through both necrosis and apoptosis of gastric mucosal cells.

gastric mucosal injury; indomethacin; aspirin; caspases; cell death


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