Protective effects of zinc chelation in traumatic brain injury correlate with upregulation of neuroprotective genes in rat brain

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 percussio...

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Bibliographic Details
Published in:Neuroscience letters 2004-01, Vol.355 (3), p.221-225
Main Authors: Hellmich, Helen L, Frederickson, Christopher J, DeWitt, Douglas S, Saban, Ricardo, Parsley, Margaret O, Stephenson, Rachael, Velasco, Marco, Uchida, Tatsuo, Shimamura, Megumi, Prough, Donald S
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Biological and medical sciences
Brain - drug effects
Brain - metabolism
Brain Injuries - drug therapy
Brain Injuries - genetics
Brain Injuries - metabolism
Cell Death - drug effects
Cell Death - physiology
Chelating Agents - metabolism
Chelating Agents - therapeutic use
Chelation Therapy - methods
Fundamental and applied biological sciences. Psychology
Gene expression
Male
Neuroprotection
Neuroprotective Agents - pharmacology
Neuroprotective Agents - therapeutic use
Rats
Rats, Sprague-Dawley
Traumatic brain injury
Up-Regulation - drug effects
Up-Regulation - physiology
Vertebrates: nervous system and sense organs
Zinc
Zinc - metabolism
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Summary: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.
ISSN:0304-3940
1872-7972
DOI:10.1016/j.neulet.2003.10.074