Involvement of cPLA2 inhibition in dexamethasone-induced thymocyte apoptosis.
作者： B. Cinque , D. Fanini , L. Di Marzio , P. Palumbo , C. La Torre
DOI: 10.1177/039463200802100307
关键词:
摘要: Various molecular mechanisms have been suggested to be involved in dexamethasone induced thymocyte apoptosis. In this study we show that pharmacological inhibition of cytoplasmic PLA2 mouse thymocytes for 18 h with arachidonyl trifluoromethyl ketone (AACOCF3) (10 microM) and palmitoyl (PACOCF3) a drastic increase apoptosis comparable observed following Dex (10(-7) M) treatment, while secretory p-bromophenacyl bromide (pBPB) (20 did not. AACOCF3-induced apoptosis, similarly Dex-induced was eliminated by cell pre-treatment the PI-PLCbeta inhibitor, U73122, but not PC-PLC inhibitor D609. These observations were corroborated ability AACOCF3, like Dex, induce rapid transient DAG generation. addition, activation acidic sphingomyelinase (aSMase) neutral (nSMase), as evaluated measurements enzyme activity extracts exposure AACOCF3 monensin inhibit apoptotic effect resulted an early ceramide levels. caspase 3, 3 prevented suggest cPLA2 may role highlight importance survival.
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