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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.
Lu, Y.Z.
Cheng, F.C.
Chu, L.F.
Hsueh, C.M.
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.
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.
ISSN: 0304-3940
DOI: 10.1016/j.neulet.2005.06.070
Appears in Collections:生命科學系所

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