Volume 22, Issue 116 (5-2015)                   Daneshvar Medicine 2015, 22(116): 11-22 | Back to browse issues page

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Neuroprotective effect of acetyl L carnitine in compression-induced model of spinal cord injury in adult rats. Daneshvar Medicine. 2015; 22 (116) :11-22
URL: http://daneshvarmed.shahed.ac.ir/article-1-1194-en.html
Abstract:   (2562 Views)
Background and Objective: Despite current efforts for treating the spinal cord injury (SCI), cell therapy and pharmacological methods have a great curing potential in this field. In this study, application of acetyl L carnitine as one of the possible pharmacologic approaches in SCI treatment was investigated. The effect of this material in adult rats suffering from spinal cord compression was examined by counting the number of motor neurons and expression of the P75 receptor and BNDF neurotrophin. Materials and Methods: In this research study, 16 adult rats were divided into 4 groups with different treating protocols: 1- laminectomy and intraperitoneal injection of acetyl L carnitine 2- laminectomy and intraperitoneal injection of acetyl L carnitine and spinal cord compression 3- laminectomy and intraperitoneal injection of saline 4- laminectomy and spinal cord compression with intraperitoneal injection of saline. After 4 weeks, the rats were sacrificed. Then, the morphometry was carried out and the spinal cord motor neurons were counted using the Cresyl fast violet technique. Expression of the P75 receptor and BNDF neurotrophin was performed by using immunohistochemical technique. Results: The obtained results indicated that the spinal cord compression reduced the number of motoneurons. The acetyl L carnitine mitigated the rate of the observed reduction in the number of motoneurons. It also helped to increase the expression of BNDF neurotrophin after spinal cord compression. Conclusion: Neuroprotective effect of acetyl L carnitine could stem from its anti-inflammatory and neuroprotective properties which are likely to be in charge of the observed decrease in the number of dead motoneurons and subsequent increase in expression of neurotrophin and reduction of oxidative stress after spinal cord compression.
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