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Nogo受体及其拮抗剂与神经节苷脂在新生大鼠HIBD中的作用

马静1,朱薇薇2,罗焕华2,姚平波2   

  1. 1. 山东大学医学院, 济南 250012; 2. 山东大学附属济南市中心医院儿科, 济南 250013
  • 收稿日期:2007-11-24 修回日期:1900-01-01 出版日期:2008-03-16 发布日期:2008-03-16
  • 通讯作者: 朱薇薇

Effect of NEP1-40 and GM-1 on hypoxic ischemic brain damage in newborn rats

MA Jing1,ZHU Wei-wei2,LUO Huan-hua2,YAO Ping-bo2   

  1. 1. School of Medicine, Shandong University, Jinan 250012, China; 2. Department of Pediatrics, Jinan Central Hospital Affiliated to Shandong University, Jinan 250013, China
  • Received:2007-11-24 Revised:1900-01-01 Online:2008-03-16 Published:2008-03-16
  • Contact: ZHU Wei-wei

摘要: 目的观察Nogo-A受体拮抗剂NEP1-40及神经节苷脂对新生大鼠缺血缺氧性脑损伤后神经再生的作用。方法将100只7日龄新生大鼠随机分为10组:在6h、24h两个时间段分别设空白对照组,假手术组,缺氧缺血性脑损伤(HIBD)模型组,HIBD后NEP140治疗组及神经节苷脂治疗组,用原位杂交的方法观察各组别Nogo-A mRNA的表达情况。结果HIBD组两时段的Nogo-mRNA表达均高于同时段空白组及假手术组,差异有统计学意义;NEP1-40治疗组能抑制HIBD后mRNA的表达,与同时段模型组对比差异有统计学意义;神经节苷脂治疗组mRNA的表达在6h时与HIBD组无明显差异,在24h时较HIBD组低但高于空白组。P值均<0.05。结论Nogo-A mRNA在缺氧缺血性脑损伤后表达显著增高,其编码的Nogo-A可抑制中枢神经损伤后的再生,NEP1-40能拮抗这一作用,从而可能在促进缺氧缺血性脑损伤后神经再生中起到作用。神经节苷脂GM-1在缺氧缺血性脑损伤后也可抑制Nogo-A mRNA的表达,有稳定细胞膜、减轻细胞水肿、促进神经再生的作用。

Abstract: To investigate the effects of NEP1-40 and GM-1 in newborn rats with hypoxic ischemic brain damage (HIBD). Methods100 rats were randomly divided into 10 groups and five groups were treated in different ways at 6h: the normal control group, the shamoperation group, the HIBD model group, the GM-1 treatment group and the NEP1-40 treatment group, and the other five groups were treated at 24 h. Contents of Nogo-A mRNA in each group were determined by the method of in situ hybridization. ResultsThe expression of Nogo-A mRNA in the HIBD groups was higher than that in the control groups, and was lower in the NEP140 groups than in the HIBD groups at both time points. There were no significant differences between the GM1 group and the HIBD group when they were treated at 6?h. However, the expression of Nogo-A mRNA was lower in the GM1 group than in the HIBD group but was higher than the normal control group. Conclusion Nogo-A mRNA is significantly increased in newborn rats with HIBD. Nogo-A encoded by mRNA can inhibit the regeneration of the central nerve after injury, and NEP1-40 could antagonize the function and promotes the regeneration. GM-1 is also able to antagonize the expression of mRNA and stabilizes the cellular membrane, eases cellular edema of the injured nerve and accelerates the regeneration of new nerves.

Key words: Rats, newborn, HypoxiaIschemia, brain, Myelinassociated glycoprotein, Ganglioside, Nogo receptor antagonists

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  • Q95.33
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