【摘 要】
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The pathology of spinal cord injury (SCI) can be divided into two phases: primary injury (mechanical damage) and secondary injury.The pathophysiological hallmarks of secondary injury include the loss
【机 构】
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Institute of Biomedical Sciences, National Sun Yat Sen University, Kaohsiung 804, Taiwan, China
【出 处】
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第三届国际神经再生高峰论坛暨第五届脊髓损伤治疗与临床试验国际交流会(INRS2013 & 5th ISCITT)
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The pathology of spinal cord injury (SCI) can be divided into two phases: primary injury (mechanical damage) and secondary injury.The pathophysiological hallmarks of secondary injury include the loss of ionic homeostasis,glutamate excitotoxicity,mitochondrial dysfunction,and microvascular disruption.Reactive oxygen species generation elicits oxidative damage and ultimately leads to secondary injury response.NERV-2 is a synthetic derivative of natural compound isolated from soft coral in Taiwan.Pilot studies indicated that NERV-2 application significantly decreased the expression of pro-inflammatory proteins in endotoxin-treated macrophages.In addition,NERV-2 supply alleviated 6-hydroxydopamine (6-OHDA)-induced cytotoxicity to human neuroblastoma SH-SY5Y cells.The aim of this study was to determine the therapeutic efficacy and anti-oxidative stress of NERV-2 treatment after SCI in rats.The contusive SCI was induced in thoracic spinal cord female Wistar rats using a NYU impactor.Saline,NERV-2,and methylprednisolone (MP; a standard SCI agent) was intrathecally injected at 1 hour after SCI for 30 days.By eriochrome cyanine R staining,the lesion area in NERV-2-treated rats was significantly reduced compared with MP- or saline-treated groups.By assessing locomotor function by Basso-Beattie-Bresnahan score,the NERV-2-treated animals exhibited significantly better locomotor function compared to MP- or saline-treated animals.Immunofluorescence analyses showed that SCI-induced microglial activation was attenuated and NADPH oxidase 2 expression was decreased in NERV-2-treated rats.In addition,NERV-2 also perturbed SCI-induced upregulation of endothelial nitric oxide synthase and nitrotyrosine production.In conclusion,NERV-2 improves the functional recovery in rats after SCI through anti-oxidative mechanism and may hold therapeutic potential for SCI therapy.
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