Publication: Early administration of methylprednisolone
decreases apoptotic cell death after spinal cord injury
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Date
2006
Authors
Vaquero, J. ; Zurita, M. ; Oya, S. ; Aguayo, C. ; Bonilla, C.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
The purpose of this study is to evaluate, in an
experimental model of spinal cord injury (SCI), the
presence of apoptotic cell death after trauma and if early
administration of a single bolus of methylprednisolone
(MP) influences apoptosis in the zone of trauma and in
adjacent spinal cord segments. For this study, a total of
96 adult female Wistar rats were subjected to spinal
contusion at the T6-T8 level, producing immediate
paraplegia. Forty-eight animals (treated group) received
a single intraperitoneal injection of MP, at a dose of 30
mg/kg body weight, 10 minutes later. Cells undergoing
apoptosis were detected by means of
immunohistochemical labeling with the monoclonal
antibody Apostain (anti-ssDNA MAb F7-26), in the
injured spinal cord tissue, both in the zone of the lesion
and in the adjacent spinal segments (rostral and caudal
zones), 1, 4, 8, 24 and 72 hours and 1 week after injury.
Apoptosis was detected in neurons and glial cells in the
zone of the lesion 1 hour after trauma, with a pattern that
showed no changes 4 hours later. Between 4 and 8 hours
postinjury, the number of apoptotic cells increased, after
which it decreased over the following days. In the
adjacent spinal segments, apoptotic cells were detected 4
hours after trauma, and increased progressively over the
remainder of the study, the number of apoptotic cells
being similar in the lesion zone and in rostral and caudal
zones one week after injury. When the group of MPtreated
animals was considered, significant decreases in
the number of apoptotic cells were detected in the lesion
zone 24 hours after injury, and in the rostral and caudal
zones, at 72 hours and at 1 week after trauma. These
findings show that early administration of a single bolus
of MP decreases apoptotic cell death after SCI,
supporting the utility of MP in reducing secondary
damage in injured spinal cord tissue.
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