EFFECTS OF ALPHA-PHENYL-N-TERT-BUTYL NITRONE (PBN) ON COMPRESSION INJURY OF RAT SPINAL-CORD

Citation
Gl. Li et al., EFFECTS OF ALPHA-PHENYL-N-TERT-BUTYL NITRONE (PBN) ON COMPRESSION INJURY OF RAT SPINAL-CORD, Free radical research, 27(2), 1997, pp. 187-196
Citations number
38
Categorie Soggetti
Biology
Journal title
ISSN journal
10715762
Volume
27
Issue
2
Year of publication
1997
Pages
187 - 196
Database
ISI
SICI code
1071-5762(1997)27:2<187:EOAN(O>2.0.ZU;2-4
Abstract
alpha-Phenyl-N-tert-butyl Nitrone (PEN) is a free radical scavenger wh ich recently has proved to be neuroprotective in experimental studies on focal cerebral ischemia and infarction. We therefore studied the ef fect of this drug in a model of moderate compression injury to rat spi nal cord at the midthoracic level. The compound was given intraperiton eally 0.5 h before (100 mg/kg b.w) and at 1.5 h (50 mg/kg b.w) and 3.5 h (50 mg/kg b.w) after compression. Treated animals and controls (veh icle alone) were allowed to survive for 1 or 9 days following trauma. The functional outcome was tested by the inclined plane method and the motor performance score. By using MAP2 immunostaining the number of n erve cell bodies in the ventral horn and the ratio of MAP2 immunostain ed area to area of whole section of the cord were assessed to detect l oss of neurons and loss of dendrites in the compressed segment. beta A PP and PGP9.5 immunostaining was used to demonstrate axonal lesions. T reated and control rats showed at day 1 when tested with the inclined plane method a marked reduction of the capacity angle. This abnormalit y recovered gradually over the following days and was normalized at da y 9. The motor performance score showed a marked reduction at day 1 wh ich almost normalized at day 9. There was no difference regarding the functional outcome between rats given PEN and controls in none one of these functional tests. The spinal cord of normal rats presented immun oreactivity to MAP2 in nerve cell bodies and dendrites but not in axon s and other structures. Following compression there was at day 1 and 9 a marked loss of MAP2 immunoreactivity in dendrites and nerve cell bo dies. We could not detect any difference between the PEN and the contr ol rats regarding the degree of cell loss or degree of reduction of de ndrite staining. No difference between the two groups was seen with th e axonal immunostainings (beta APP and PGP9.5). In conclusion, our stu dy did not reveal any neuroprotective effect of PEN on the functional outcome and morphology (immunostaining to MAP2, beta APP and PGP9.5) i n this model of moderate compression trauma to rat spinal cord.