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【目的】探讨Nogo-A及其受体拮抗剂NEP1-40在新生大鼠缺氧缺血性脑损伤修复中的作用。【方法】将64只新生7日龄大鼠按6h、24h两个时段随机分为8组,空白对照组、HIBD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0.9%氯化钠0.25mL/kg、0.9%氯化钠0.25mL/kg、NEP1-4010mg/kg、GM-120mg/kg。原位杂交法观察各组Nogo-A的表达情况,透射电镜观测脑组织超微结构的动态变化。【结果】Nogo-A阳性细胞的表达:对照组两时段细胞数均随着时间的延长而略增加,两时段比较无统计学意义(P均>0.05)。HIBD组两时段均高于同时段对照组,NEP1-40组表达明显减少,与同时段HIBD组对比有显著统计学意义;GM-1组较HIBD组低,但高于NEP1-40组。NEP1-40及GM-1治疗后脑组织超微结构得以不同程度恢复(P均<0.05)。【结论】Nogo-A可抑制中枢神经损伤后的再生,NEP1-40能拮抗这一作用并促进神经元再生,GM-1在HIBD神经损伤修复中亦能促进再生。
【Aim】 To investigate the role of Nogo-A and its receptor antagonist NEP1-40 in the repair of hypoxic-ischemic brain damage in neonatal rats. 【Methods】 Sixty-four neonatal 7-day-old rats were randomly divided into 8 groups at 6 h and 24 h. The control group, HIBD model group (HIBD group), NEP1-40 treatment group (NEP1-40 group) (GM-1 group), followed by intraperitoneal injection of 0.9% sodium chloride 0.25mL / kg, 0.9% sodium chloride 0.25mL / kg, NEP1-4010mg / kg, GM-120mg / kg. In situ hybridization was used to observe the expression of Nogo-A in each group. The ultrastructure of brain tissue was observed by transmission electron microscope. [Results] The expression of Nogo-A positive cells: The number of cells in both control groups increased slightly with the time prolonging. There was no significant difference between the two periods (all P> 0.05). Compared with HIBD group, the expression of NEP1-40 in HIBD group was significantly higher than that of HIBD group in the same period. The expression of NEP1-40 in HIBD group was lower than that in HIBD group, but higher than that in NEP1-40 group. The ultrastructures of brain tissue recovered after NEP1-40 and GM-1 treatment (P <0.05). 【Conclusion】 Nogo-A can inhibit the regeneration after CNS injury. NEP1-40 can antagonize this effect and promote the regeneration of neurons. GM-1 can also promote the regeneration of HIBD nerve injury.