Laboratory Study
Elevation of neuron-specific enolase and S-100β protein level in experimental acute spinal cord injury

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Abstract

We evaluated the protein levels of neuron-specific enolase (NSE) and S-100β in serum and cerebrospinal fluid (CSF) in an animal model of acute spinal cord injury and ascertained their relevance. Spinal cord injury was induced at the T8 level in rats. Enzyme-linked immunosorbent assay was used to measure the protein levels of NSE and S-100β in both serum and CSF at different time points (30 min, 2 h, 6 h, 12 h and 24 h after induction of spinal cord injury). There existed a significant correlation between neurological deficits and the severity of spinal cord injury (p < 0.05). Compared with the control group, the protein levels of NSE and S-100β in serum and CSF significantly increased from 2 h after injury (p < 0.05) and reached a maximum at 6 h. Within a certain time window, the protein levels of NSE and S-100β in serum and CSF were closely related to the severity of injury level (p < 0.05). The protein levels of NSE and S-100β in serum and CSF significantly increased after experimental spinal cord injury in a time-dependent manner and thus may be considered specific biomarkers for acute spinal cord injury.

Introduction

Traumatic spinal cord injury (SCI) often results in complete or partial motor and sensory neurological deficits under the level of the injury. Much effort has been expended in attempts to evaluate SCI severity and subsequent recovery potential. But there is still no consensus on which clinical diagnostic tests could be applied to reliably indicate the subclinical neurophysiological changes occuring in the spinal cord during the acute phase, and this presents a major obstacle in predicting the progression of cell death as well as tissue destruction in SCI cases. Recently, there has been growing interest in serum biomarkers as indicators of tissue destruction in central nervous system (CNS) diseases. Several previous studies have indicated that monitoring the levels of neuron- or astroglia-specific proteins in the serum and cerebrospinal fluid (CSF) might turn out to be a useful approach for evaluating the severity of CNS injury (e.g. traumatic brain injury, cerebral infraction, intracranial hemorrhage, and SCI). The aim of this study was to ascertain the relationship between protein levels of neuron-specific enolase (NSE) and S-100β in serum and CSF and the severity of acute SCI in an animal model.

Section snippets

Experimental animals and grouping

We used 80 adult male Sprague-Dawley rats weighing 200 ± 20 g (provided by the Experimental Animal Center of Zhejiang University School of Medicine) for this study. Rats were randomly divided into four groups: control group, mild SCI group, moderate SCI group and severe SCI group (20 rats per group).

SCI model induction

Rats were anesthetized with 1% sodium pentobarbital (40 mg/kg intraperitoneally). After dorsal laminectomy of the T8 and T9 vertebrae to expose the spinal cord, 60 rats (the mild, moderate and severe

Neurological scoring

There were significant differences between the SCI group and the control group with respect to neurological score as determined using the modified Tarlov method and CBS (p < 0.05). A higher SCI injury grade correlated with poorer neurological score (p < 0.05) (Table 1).

NSE level

Over the course of the experiment, changes in the serum NSE protein level were similar to those that occurred in the CSF. In the control group, the NSE level remained low at all time points. At 30 min after injury, the NSE level in

Discussion

Acute spinal cord injury is a common cause of mortality and morbidity. Many neuropathological, neuroendocrinological and neurobiological alterations happen during the acute phase of SCI.[5], [6], [7] Successful management of SCI necessitates an appropriate diagnostic standard for the acute phases after injury. Neurological examinations provide a general indication of spinal cord neurological function, but are unreliable, especially during the acute phase (first 24 h) after SCI as a result of

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