| Literature DB >> 14732471 |
Helen L Hellmich1, Christopher J Frederickson, Douglas S DeWitt, Ricardo Saban, Margaret O Parsley, Rachael Stephenson, Marco Velasco, Tatsuo Uchida, Megumi Shimamura, Donald S Prough.
Abstract
Chelation of excessive neuronal zinc ameliorates zinc neurotoxicity and reduces subsequent neuronal injury. To clarify the molecular mechanisms of this neuroprotective effect, we used a focused cDNA array of stress-response genes with zinc chelation (calcium EDTA) in our rat model of fluid percussion brain injury at 2 h, 24 h, and 7 days after injury. In parallel experiments, we compared neuronal cell death in TUNEL-stained brain sections in traumatized rats with and without calcium EDTA treatment. Zinc chelation induced the expression of several neuroprotective genes; neuroprotective gene expression correlated with substantially decreased numbers of TUNEL-positive cells.Entities:
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Year: 2004 PMID： 14732471 DOI： 10.1016/j.neulet.2003.10.074
Source DB: PubMed Journal: Neurosci Lett ISSN： 0304-3940 Impact factor: 3.046