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Article type: Research Article
Authors: Li, Xiuming | Oudega, Martin | Dancausse, Hector A. | Levi, Allan D.O.
Affiliations: The Miami Project te Cure Paralysis, Department of Neurosurgery, University of Miami School of Medicine, Lois Pope LIFE Center, Miami, Florida 33136, USA
Note: [] Corresponding author: Allan D.O. Levi MD, PhD., The Miami Project to Cure Paralysis, University of Miami School of Medicine, Lois Pope LIFE Center, 1095 NW 14th terrace, R-48, Miami, FL 33101. Tel.: +1 305 243 2088; Fax: +1 305 243 6017; E-mail: [email protected].
Abstract: Purpose: Caspase-3 is known as a crucial effector for apoptotic cell death. Apoptosis has recently been recognized as an important cell death mechanism after spinal cord injury (SCI). This study attempts to define the effect of methylprednisolone (MP) on the activation of caspase-3 in the lesioned area following SCI. Methods: Forty-eight rats with a complete transection of the thoracic spinal cord received a placebo or MP (30 mg/kg, iv.) at 5 min, 2 and 4 h post-injury and were then sacrificed at 12, 24 h, 3 or 7 days thereafter. Results: Caspase-3 positive cells in the lesioned area were immunocytochemically observed in both cord stumps and decreased in number with increasing distance from the lesion site. More caspase-3 positive cells were present in the MP-treated group than the control group at all time points, but the differences were not statistically significant. Conclusion: These results suggest that the MP-induced decrease of tissue loss following SCI may not involve a reduction of apoptotic cell death.
Keywords: apoptosis, caspase-3, immunocytochemistry, methylprednisolone, secondary damage, spinal cord injury
Journal: Restorative Neurology and Neuroscience, vol. 17, no. 4, pp. 203-209, 2000
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