Modulation of inflammatory response after spinal cord trauma with deferoxamine, an iron chelator

Irene Paterniti, Emanuela Mazzon, Esposito Emanuela, Rosanna D. Paola, Maria Galuppo, Placido Bramanti, Salvatore Cuzzocrea

Research output: Contribution to journalArticlepeer-review


The standard iron-chelator deferoxamine is known to reduce neurological deficits. The aim of the present study was to evaluate the contribution of deferoxamine in the secondary damage in experimental spinal cord injury (SCI) in mice, induced by the application of vascular clips to the dura via a four-level T5T8 laminectomy. SCI resulted in production of inflammatory mediators, tissue damage and apoptosis. Deferoxamine treatment 30 min before and 1 and 6 h after the SCI significantly reduced: (1) GFAP immunoreactivity, (2) neutrophil infiltration, (3) NF-κB activation, (4) iNOS expression, (5) nitrotyrosine and MDA formation, (6) DNA damage (methyl green pyronin staining and PAR formation and (7) apoptosis (TUNEL staining, FasL, Bax and Bcl-2 expression, S-100 expression). Moreover, deferoxamine significantly ameliorated the recovery of limb function (evaluated by motor recovery score). Taken together, the results clearly demonstrate that deferoxamine treatment reduces the development of inflammation and tissue injury associated with spinal cord trauma.

Original languageEnglish
Pages (from-to)694-709
Number of pages16
JournalFree Radical Research
Issue number6
Publication statusPublished - 2010


  • Apoptosis
  • Inflammatory mediators
  • SCI
  • Tissue damage

ASJC Scopus subject areas

  • Biochemistry


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