Abstract
ObjectiveErythropoietin (EPO) is a clinically available hematopoietic cytokine. EPO has shown beneficial effects in the context of spinal cord injury and other neurological conditions. The aim of this study was to evaluate the effect of EPO on a rat model of spinal cord compression-induced cervical myelopathy and to explore the possibility of its use as a pharmacological treatment.MethodsTo develop the compression-induced cervical myelopathy model, an expandable polymer was implanted under the C5-C6 laminae of rats. EPO administration was started 8 weeks after implantation of a polymer. Motor function of rotarod performance and grip strength was measured after surgery, and motor neurons were evaluated with H-E, NeuN and choline acetyltransferase staining. Apoptotic cell death was assessed with TUNEL and Caspase-3 staining. The 5HT, GAP-43 and synaptophysin were evaluated to investigate the protection and plasticity of axons. Amyloid beta precursor protein (APP) was assessed to evaluate axonal injury.To assess transfer of EPO into spinal cord tissue, the EPO levels in spinal cord tissue were measured with an ELISA for each group after subcutaneous injection of EPO.ResultsHigh-dose EPO maintained motor function in the compression groups. EPO significantly prevented the loss of motor neurons and significantly decreased neuronal apoptotic cells. Expression of 5HT and synaptophysin was significantly preserved in the EPO group. APP expression was partly reduced in the EPO group. The EPO levels in spinal cord tissue were significantly higher in the high-dose EPO group than other groups.ConclusionEPO improved motor function in rats with compression-induced cervical myelopathy. EPO suppressed neuronal cell apoptosis, protected motor neurons, and induced axonal protection and plasticity. The neuroprotective effects were produced following transfer of EPO into the spinal cord tissue. These findings suggest that EPO has high potential as a treatment for degenerative cervical myelopathy.
Highlights
As the population ages, degenerative changes in the cervical spine progress
The neuroprotective effects were produced following transfer of EPO into the spinal cord tissue. These findings suggest that EPO has high potential as a treatment for degenerative cervical myelopathy
The present study demonstrated that EPO improved locomotor functions and preserved motor neurons and axons, even in developing myelopathy due to spinal cord compression
Summary
The spinal canal gradually narrows due to cervical spondylosis, disc hernia, and ossification of the posterior longitudinal ligament [1] [2]. This chronic compression of the cervical spinal cord causes degenerative cervical myelopathy. Mechanical stress as a consequence of focal compression, which induces spinal cord ischemia at the compressed segment, is an important component in the pathogenesis of degenerative cervical myelopathy [3]. At this time, surgical decompression is often performed to treat degenerative cervical myelopathy [4] [5] [6]. There is no accredited medical treatment which improve the neurological status in patients with worsening degenerative cervical myelopathy
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