Authors: Viera Danielisová Miroslav Gottlieb Miroslava Némethová Petra Kravčuková Iveta Domoráková Eva Mechírová Jozef Burda
Publish Date: 2009/03/04
Volume: 29, Issue: 6-7, Pages: 871-878
Abstract
Aims The present study was undertaken to evaluate possible neuroprotective effect of bradykinin against delayed neuronal death in hippocampal CA1 neurons if applied two days after transient forebrain ischemia in the rat Methods Transient forebrain ischemia was induced in male Wistar rats by fourvessel occlusion for 8 min To assess efficacy of bradykinin as a new stressor for delayed postconditioning we used two experimental groups of animals ischemia 8 min and 3 days of survival and ischemia 8 min and 3 days of survival with ip injection of bradykinin 150 μg/kg applied 48 h after ischemia Results We found extensive neuronal degeneration in the CA1 region at day 3 after ischemia/reperfusion The postischemic neurodegeneration was preceded by increased activity of mitochondrial enzyme MnSOD in cytoplasm indicating release of MnSOD from mitochondria in the process of delayed neuronal death Increased cytosolic cytochrome c and subsequently caspase3 activation are additional signs of neuronal death via the mitochondrial pathway Bradykinin administration significantly attenuated ischemiainduced neuronal death and also suppressed the release of MnSOD and cytochrome c and prevented caspase3 activation Conclusions Bradykinin can be used as an effective stressor able to prevent mitochondrial failure leading to apoptosislike delayed neuronal death in postischemic rat hippocampus
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