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• W2011362522 abstract "Nonsteroidal anti-inflammatory drugs (NSAIDs), widely used in clinical practice, cause adverse effects in the gastrointestinal tract. These effects have been attributed to mechanisms such as drug-induced cyclooxygenase inhibition, oxidative stress, mitochondrial dysfunction and changes in cell membrane lipids. Our previous study showed that indomethacin (an NSAID commonly used in toxicity studies) caused activation of cytosolic phospholipase A2 (cPLA2) in the rat small intestine. We hypothesized that activation of cPLA2 is an important event in the pathogenesis of indomethacin-induced damage in enterocytes. To test this, we incubated enterocyte-like Caco-2 cells with indomethacin, with and without pretreatment with methyl arachidonyl fluorophosphonate (MAFP), an inhibitor of cPLA2. Cells treated with indomethacin showed decreased viability and evidence of oxidative stress and morphological cell damage. Phospholipids were degraded in these cells, with increases in the levels of lysophospholipids and arachidonic acid. There was no evidence of apoptosis in the cells in response to the drug. Pretreatment of the cells with MAFP attenuated the drug-induced effects seen. This shows that activation of phospholipase A2 appears to be an important event in the pathogenesis of indomethacin-induced damage in Caco-2 cells. To our knowledge, this is the first report that implicates the involvement of this enzyme in NSAID-induced enteropathy." @default.
• W2011362522 created "2016-06-24" @default.
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• W2011362522 date "2009-08-01" @default.
• W2011362522 modified "2023-09-26" @default.
• W2011362522 title "Activation of phospholipase A2 is involved in indomethacin-induced damage in Caco-2 cells" @default.
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• W2011362522 doi "https://doi.org/10.1016/j.tiv.2009.05.008" @default.
• W2011362522 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19470405" @default.
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