机构地区:[1]Wuxi Hospital of Traditional Chinese Medicine, Institute of Orthopedics and Traumatology of Nanjing University of Chinese Medicine [2]Nanjing University of Chinese Medicine
出 处:《Neural Regeneration Research》2015年第2期225-229,共5页中国神经再生研究(英文版)
基 金:financially supported by a grant from the Natural Science Foundation of Jiangsu Province,No.BK2011180;Ordinary University Graduate Student Scientific Research Innovation Projects of Jiangsu Province,No.CXZZ13-0614,CXZZ12-0609
摘 要:The mechanism involved in neural regeneration after spinal cord injury is unclear. The my-elin-derived protein Nogo-A, which is speciifc to the central nervous system, has been identiifed to negatively affect the cytoskeleton and growth program of axotomized neurons. Studies have shown that Nogo-A exerts immediate and chronic inhibitory effects on neurite outgrowth.In vivo, inhibitors of Nogo-A have been shown to lead to a marked enhancement of regenerative axon extension. We established a spinal cord injury model in rats using a free-falling weight drop device to subsequently investigate Nogo-A expression. Nogo-A mRNA and protein expression and immunoreactivity were detected in spinal cord tissue using real-time quantitative PCR, immu-nohistochemistry and western blot analysis. At 24 hours after spinal cord injury, Nogo-A protein and mRNA expression was low in the injured group compared with control and sham-operated groups. The levels then continued to drop further and were at their lowest at 3 days, rapidly rose to a peak after 7 days, and then gradually declined again after 14 days. These changes were observed at both the mRNA and protein level. The transient decrease observed early after injury followed by high levels for a few days indicates Nogo-A expression is time dependent. This may contribute to the lack of regeneration in the central nervous system after spinal cord injury. The dynamic varia-tion of Nogo-A should be taken into account in the treatment of spinal cord injury.The mechanism involved in neural regeneration after spinal cord injury is unclear. The my-elin-derived protein Nogo-A, which is speciifc to the central nervous system, has been identiifed to negatively affect the cytoskeleton and growth program of axotomized neurons. Studies have shown that Nogo-A exerts immediate and chronic inhibitory effects on neurite outgrowth.In vivo, inhibitors of Nogo-A have been shown to lead to a marked enhancement of regenerative axon extension. We established a spinal cord injury model in rats using a free-falling weight drop device to subsequently investigate Nogo-A expression. Nogo-A mRNA and protein expression and immunoreactivity were detected in spinal cord tissue using real-time quantitative PCR, immu-nohistochemistry and western blot analysis. At 24 hours after spinal cord injury, Nogo-A protein and mRNA expression was low in the injured group compared with control and sham-operated groups. The levels then continued to drop further and were at their lowest at 3 days, rapidly rose to a peak after 7 days, and then gradually declined again after 14 days. These changes were observed at both the mRNA and protein level. The transient decrease observed early after injury followed by high levels for a few days indicates Nogo-A expression is time dependent. This may contribute to the lack of regeneration in the central nervous system after spinal cord injury. The dynamic varia-tion of Nogo-A should be taken into account in the treatment of spinal cord injury.
关 键 词:nerve regeneration spinal cord injury CONTUSION NOGO-A axon growth IMMUNOHISTO-CHEMISTRY fluorescent quantitative PCR neural regeneration
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