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作 者:张文明[1] 涂致远[1] 朱维钦[1] 林建华[1]
机构地区:[1]福建医科大学附属第一医院骨科,福州市350005
出 处:《实用医学杂志》2007年第12期1798-1800,共3页The Journal of Practical Medicine
基 金:福建省自然科学基金资助项目(编号:C0210010)
摘 要:目的:观察臂丛根性撕脱伤后脊髓源性神经干细胞(NSC)脊髓内移植对脊髓前角运动神经元一氧化氮合酶(NOS)表达的影响。方法:取新生鼠脊髓,分离培养脊髓源性NSC,SD大鼠60只,随机分成3组,制备后路C5~7神经根撕脱伤动物模型,实验组移植脊髓源性NSC悬液于C6脊髓节段,对照组移植灭活的NSC悬液,单纯组不作移植作为空白对照。术后1、2、4、8、12周取脊髓标本进行组织学、免疫组化染色观察和运动神经元计数。结果:臂丛根性撕脱伤后脊髓前角运动神经元表达NOS;脊髓源性NSC移植手术后2、4、8周实验组脊髓运动神经元NOS的表达低于对照组和单纯组;脊髓源性NSC移植术后2、4、8、12周实验组运动神经元的存活率高于对照组和单纯组;对照组和单纯组NOS的表达和运动神经元的存活率无明显差异。结论:臂丛根性撕脱伤后脊髓源性NSC脊髓内移植可减少脊髓前角运动神经元NOS表达,对脊髓运动神经元的继发性死亡的保护机制可能与抑制受损运动神经元NOS表达有关。To explore the effects of intraspinal transplant of neural stem cells (NSCs) on nitricoxidesynthase (NOS) expressions in motor neurons in the ventral horn of the spinal cord after brachial plexus injury. Methods NSCs were isolated from the spinal cord of neonate rats and then cultured. A murine model of avulsion in cervical nerve roots C^5~7 was constructed on 60 SD rats. The rats were then randomly assigned to receive transplant of NSCs at C6 level of the cervical spine (experimental group), transplant of inactive NSCs (control group), or no transplant (blank group). Histological examination, immunohistochemistry assay, and motor neuron count were performed on the injured cervical cord on weeks 1, 2, 4, 8, and 12 of the procedure. Results NOS expressed in motor neurons in the ventral horn of the spinal cord after brachial plexus injury, The levels of NOS expressions were lower in the experimental group than those in the control or blank group on weeks 2, 4, and 8. The survival rate of the motor neurons in the experimental group was higher than that in the control or blank group on weeks 2, 4, 8, and 12, NOS expressions and the survival rate of the motor neurons did not differ significantly between the control group and the blank group, Conclusion Intraspinal transplant of NSCs after brachial plexus injury may decrease the NOS expressions in motor neurons in the ventral horn, which may be involved in protection of the secondary motor neuron death.
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