PMID- 17184187
OWN - NLM
STAT- MEDLINE
DCOM- 20070319
LR  - 20131121
IS  - 0897-7151 (Print)
IS  - 0897-7151 (Linking)
VI  - 23
IP  - 12
DP  - 2006 Dec
TI  - Mn (III) tetrakis (4-benzoic acid) porphyrin administered into the intrathecal 
      space reduces oxidative damage and neuron death after spinal cord injury: a 
      comparison with methylprednisolone.
PG  - 1766-78
AB  - The metalloporphyrin Mn (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP) is a 
      cell-permeable superoxide dismutase mimetic and a broad-spectrum scavenger of 
      reactive species. Since MnTBAP may not cross the blood-brain barrier, this study 
      evaluated the therapeutic potential of MnTBAP to treat spinal cord injury (SCI; 
      25 g x cm) by directly administering it into the intrathecal space of the rat 
      spinal cord. The cells in spinal sections removed at 24 h post-SCI were 
      immunohistochemically stained with anti-4-hydroxynonenal (HNE), a marker of 
      membrane lipid peroxidation (MLP); anti-nitrotyrosine (Ntyr), a marker of protein 
      nitration; and anti-neuron-specific enolase (NSE) antibodies. Immunostained 
      neurons were counted for quantitative evaluation. Pre-treatment 30 min before SCI 
      with 1 mg/kg MnTBAP or 4-h post-SCI treatment with 2.5 mg/kg MnTBAP administered 
      into the intrathecal space significantly reduced MLP and protein nitration, and 
      increased the number of surviving neurons compared to vehicle controls. However, 
      post-SCI treatment with a standard regimen of methylprednisolone sodium succinate 
      (MPSS; 30 mg/kg followed by 5.4 mg/kg for maintenance, iv administration), the 
      only drug used for clinical treatment of SCI, not only did not reduce MLP and 
      neuron loss, it increased protein nitration compared with vehicle controls 
      (two-way analysis of variance [ANOVA] followed by the Tukey test). These results 
      demonstrate that pre- and post-intrathecal treatments with the low doses of 
      MnTBAP provide sustained neuroprotection by preventing oxidative stress and that 
      post-treatment with MnTBAP is superior to post-treatment with MPSS in preventing 
      oxidative stress and resulting neuron loss.
FAU - Hachmeister, Jorge E
AU  - Hachmeister JE
AD  - Department of Neurology, University of Texas Medical Branch, Galveston, Texas 
      77555-0881, USA.
FAU - Valluru, Lokanatha
AU  - Valluru L
FAU - Bao, Feng
AU  - Bao F
FAU - Liu, Danxia
AU  - Liu D
LA  - eng
GR  - R01 NS 044324/NS/NINDS NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - J Neurotrauma
JT  - Journal of neurotrauma
JID - 8811626
RN  - 0 (Free Radical Scavengers)
RN  - 0 (Metalloporphyrins)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (manganese(III)-tetrakis(4-benzoic acid)porphyrin)
RN  - 5GMR90S4KN (Methylprednisolone Hemisuccinate)
SB  - IM
MH  - Animals
MH  - Apoptosis/*drug effects
MH  - Dose-Response Relationship, Drug
MH  - Drug Administration Schedule
MH  - Free Radical Scavengers/*administration & dosage
MH  - Injections, Spinal
MH  - Male
MH  - Metalloporphyrins/*administration & dosage
MH  - Methylprednisolone Hemisuccinate/therapeutic use
MH  - Neuroprotective Agents/therapeutic use
MH  - Oxidative Stress/*drug effects
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Spinal Cord Injuries/*drug therapy/metabolism/pathology
EDAT- 2006/12/23 09:00
MHDA- 2007/03/21 09:00
CRDT- 2006/12/23 09:00
PHST- 2006/12/23 09:00 [pubmed]
PHST- 2007/03/21 09:00 [medline]
PHST- 2006/12/23 09:00 [entrez]
AID - 10.1089/neu.2006.23.1766 [doi]
PST - ppublish
SO  - J Neurotrauma. 2006 Dec;23(12):1766-78. doi: 10.1089/neu.2006.23.1766.