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|標題:||Bax-regulated mitochondria-mediated apoptosis is responsible for the in vitro ischemia induced neuronal cell death of Sprague Dawley rat||作者:||Lin, C.H.
|關鍵字:||in vitro ischemia;neuronal cell death;apoptosis;mitochondria;Bax;caspases;furosemide;ZVAD-fmk;permeability transition;cytochrome-c;membrane;damage;activation;mechanisms;necrosis;channel||Project:||Neuroscience Letters||期刊/報告no：:||Neuroscience Letters, Volume 387, Issue 1, Page(s) 22-27.||摘要:||
An in vitro ischemia model was used to determine the molecular mechanisms responsible for the ischemia-induced neuronal cell death. Additionally, the neuronal protective mechanisms of anti-apoptotic drugs against ischemia were also evaluated. In this study, the primary neuronal cultures were incubated in an anoxic chamber with 95% of N-2 and 5% of CO2 for various times. The death rate, degree of the apoptotic damage, reduction of mitochondrial membrane potential, translocation of Bax, release of cytochrome C and activation of caspase-9 and -3 were determined at each time point. Results showed that a Bax-regulated mitochondria- mediated apoptosis is responsible for the in vitro ischemia-induced neuronal death. Reduction in mitochondrial membrane potential plays no role in triggering this apoptosis. Furthermore, the anti-apoptotic drugs: furosemide (a Bax blocker) and ZVAD-fmk (caspase inhibitor) but not cyclosporine A (a NIPT pore blocker), significantly protected the neurons against ischemia-induced damage. This provides an additional consideration in the future selection of new anti-ischemic drugs. (C) 2005 Elsevier Ireland Ltd. All rights reserved.
|Appears in Collections:||生命科學系所|
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