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机构地区:[1]山东大学附属济南市中心医院小儿内科,250013
出 处:《当代医学》2012年第19期4-6,共3页Contemporary Medicine
摘 要:目的探讨早期应用Nogo-A受体拮抗剂NEP1-40对大鼠缺氧缺血性脑损伤(HIBD)轴突再生的影响。方法将96只新生7日龄Wistar大鼠随机分为24h、72h和7d时段的对照组、缺氧缺血性脑损伤模型组(HIBD组)、NEP1-40治疗组(NEP1-40组)及神经节苷脂治疗组(GM-1组),依次分别腹腔注射生理盐水、NEP1-40、GM-1,视分组情况连用72h和7d。用免疫组化法(SP法)观察各组Nogo-A蛋白的表达水平及轴突生长情况。P<0.05为差异有统计学意义。结果 HIBD组在24h、72h和7d的Nogo-A蛋白表达均高于同时点的对照组(P<0.05),呈现增加的趋势。NEP1-40治疗组和GM-1治疗组Nogo-A蛋白表达均低于同时段模型组(P<0.05);NEP1-40治疗组Nogo-A蛋白表达弱于同时段的GM-1组,差异有显著性(P<0.05)。电镜下,模型组神经元胞膜破裂,核固缩,胞质溶解,可见较多的凋亡小体,GM-1组72h及7d胶质细胞增生,轴突再生不明显,而NEP1-40组72h及7d胶质细胞数量增加,轴突再生明显。结论中枢神经系统损伤后,中枢神经抑制因子Nogo蛋白表达增加,抑制了轴突的再生。NEP1-40可拮抗这一作用,发挥促脑损伤后神经的修复与再生作用。Objective To observe the effect of Nogo-A receptor antagonist NEP1-40 on neuronal regeneration of newbom rats atter hypoxia-isehemia. Methods 96 new born Wrstar rats of 7 days were randomly divided into 4 groups: the control group, the HIBD group, the NEP1-40 group and the GM-1 group, respectively. Rats in the control group and HIBD group were injected with saline by intmperitoneal injection, while NEP1-40 group and GM-1 group were administrated respectively with NEP1-40 and GM-1 for 72h and 7 days. Immunohistochemical staining (SP) was adopted to observe the level ofNogo-A proten expression as well as the growth of axorL P〈0.05 is of statistical significance. Results ARe, injury, the level of Nogo-A protein expression in 24h, 7211 and 7days in the HIBD group was higher than that in the control groups at the same time point (P〈0.05), and showed an incremental tendency. While the level of Nogo-A protein expression was lower in the NEP1-40 group than that of the GM-1 group at corresponding time point, and the difference is significant (P〈0.05). Under electronic microscopy the cytolemma of neurons were broken, pyknosis, basic cytoplasm soluted, Many apoptotic bodies has been observed in the model group, while in the NEP 1-40 group showed an increasing of the glial cells amount and an obvious regeneration of axon. Conclusion After injury of the central nervous system (CNS), the Nogo-A protein expression of the CNS inhibitory factoris increased and the regeneration of the axon is restrained. NEP1-40 can against this effect and promote the repair of regeneration of the nerve after injury.
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