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

Helen L. Hellmich, Christopher J. Frederickson, Douglas S. DeWitt, Ricardo Saban, Margaret O. Parsley, Rachael Stephenson, Marco Velasco, Tatsuo Uchida, Megumi Shimamura, Donald S. Prough

Research output: Contribution to journalArticle

47 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)221-225
Number of pages5
JournalNeuroscience Letters
Volume355
Issue number3
DOIs
StatePublished - Jan 30 2004

Keywords

  • Apoptosis
  • Gene expression
  • Neuroprotection
  • Traumatic brain injury
  • Zinc

ASJC Scopus subject areas

  • Neuroscience(all)

Fingerprint Dive into the research topics of 'Protective effects of zinc chelation in traumatic brain injury correlate with upregulation of neuroprotective genes in rat brain'. Together they form a unique fingerprint.

  • Cite this