文章摘要
钱旭东 ,王东 ,徐倩倩 ,李国芸 ,王红梅 ,张晓璇 ,马征.艾地苯醌改善血管性痴呆大鼠认知功能及其对 海马区生长相关蛋白-43和突触素P38表达的影响[J].神经损伤功能重建,2019,14(12):611-613
艾地苯醌改善血管性痴呆大鼠认知功能及其对 海马区生长相关蛋白-43和突触素P38表达的影响
Effect of Idebenone on Cognitive Function and Expression of Hippocampus GAP-43 andP38 in Vascular Dementia Rats
  
DOI:
中文关键词: 艾地苯醌  突触再生  血管性痴呆
英文关键词: idebenone  synaptic regeneration  vascular dementia
基金项目:2018 年承德市科学 技术研究与发展计划 项目(No.201804A08 0)
作者单位
钱旭东a ,王东a ,徐倩倩a ,李国芸b ,王红梅a ,张晓璇a ,马征a 承德市医学院附属医 院 a.神经内科b.呼 吸内科 
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中文摘要:
      目的:探讨艾地苯醌对血管性痴呆(VD)大鼠认知功能的作用,并初步探讨其机制。方法:SD大鼠 60只随机均分为3组:假手术组、模型组和艾地苯醌组,各20只。采用改良双血管阻断(2-VO)法建立大 鼠VD 模型,艾地苯醌组大鼠腹腔注射艾地苯醌,10 mg/kg,1次/d,连续给药30 d;模型组及假手术组腹 腔注射等量生理盐水。采用水迷宫评价各组大鼠学习、记忆能力;免疫组化测定海马生长相关蛋白-43 (GAP-43)、突触素P38表达;透射电镜观察突触超微结构的改变。结果:模型组逃避潜伏期长于假手术 组和艾地苯醌组(P<0.05),穿越原平台次数少于假手术组和艾地苯醌组(P<0.05);艾地苯醌组逃避潜 伏期和穿越原平台次数与假手术组差异无统计学意义(P>0.05)。模型组GAP-43和触素P38蛋白的表 达水平均低于其他2组(P<0.05);艾地苯醌组GAP-43和触素P38蛋白的表达水平均高于其他2组(P< 0.05)。电镜下可见模型组大鼠海马区突触结构受损,艾地苯醌组大鼠海马组织区突触数量丰富,结构 基本完整。结论:艾地苯醌可改善VD大鼠的学习和记忆功能,其机制可能与增强突触相关蛋白GAP-43 和突触素P38的表达有关。
英文摘要:
      To investigate the effects of idebenone on cognitive function and expression of growth associated protein-43 (GAP-43) and synaptophysin P38 in the hippocampus of vascular dementia (VD) rats. Methods: Sixty SD rats were randomly divided into the sham operation group, model group, and idebenone group with 20 rats in each group. The VD rat model was established by modified 2-vessel occlusion (2-VO) method. Idebenone group rats were given intraperitoneal injections of idebenone at 10 mg/ kg once per day for 30 consecutive days, and model group and sham operation group rats were given equivalent doses of normal saline. The differences in learning and memory capabilities were evaluated by water maze. The expression of GAP-43 and synaptophysin P38 in the hippocampus was measured by immunohistochemistry. The ultrastructure of synapses was observed by transmission electron microscopy. Results: The model group showed increased escape latency and decreased platform crossings in the water maze compared to those in the sham operation and idebenone groups (both P<0.05). The escape latency and platform crossings of the idebenone group and sham operation group showed no significant difference (P> 0.05). Compared with that of sham operation group and idebenone group rats, the GAP-43 and synaptophysin P38 expression in the hippocampus of model group rats was decreased (P<0.05). Hippocampus expression of GAP-43 and synaptophysin P38 in idebenone group rats was increased compared to that of sham operation group and model group rats (P<0.05). Electron microscopy showed that in model group rats, synaptic structure in the hippocampus was damaged while in idebenone group rats, synapses in the hippocampus were abundant in quantity and complete in structure. Conclusion: Idebenone may improve learning and memory capabilities in VD rats via mechanisms that involve up-regulating GAP-43 and synaptophysin P38 expression.
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