有氧训练对阿尔茨海默病模型大鼠海马齿状回神经发生的影响

被引：6

作者：

史兆春 ^{[1
]}

吴婷 ^{[1
]}

乔莉 ^{[2
]}

董海蓉 ^{[1
]}

李敏 ^{[1
]}

机构：

[1] 南京医科大学第一附属医院神经内科

[2] 南京医科大学第一附属医院急诊内科

来源：

中国临床神经科学 | 2011年 / 19卷 / 03期

关键词：

阿尔茨海默病; 神经发生; 5-溴脱氧尿嘧啶核苷; 微管相关蛋白;

D O I：

暂无

中图分类号：

R749.1 [脑器质性精神障碍];

学科分类号：

摘要：

目的:观察有氧训练对β淀粉样蛋白25-35(Aβ25-35)诱导的阿尔茨海默病(AD)大鼠齿状回(DG)神经发生的影响。方法:SD大鼠48只,随机分为假手术组(侧脑室注射生理盐水),有氧训练组(侧脑室注射Aβ25-35+4周有氧训练)和实验组(侧脑室注射Aβ25-35)。3组大鼠行Morris水迷宫行为学检测,免疫组织化学方法检测海马DGBrdU阳性细胞数,以确定有氧训练对细胞存活的影响;微管相关蛋白免疫组化染色观察新生神经元的突起生长。结果:①与假手术组比,实验组逃避潜伏期显著延长(P<0.05);有氧训练组与实验组比,逃避潜伏期明显缩短(P<0.05);有氧训练组逃避潜伏期与假手术组比,差异无统计学意义。②与假手术组比,实验组DGBrdU阳性细胞数显著减少(P<0.05)。③与假手术组比,实验组DG新生神经元突起的数量明显减少(P<0.05)。④与实验组比,有氧训练可改善DGBrdU阳性细胞的显著减少(P<0.05)、保护神经元突起的生长(P<0.05)。结论:Aβ25-35能诱导AD大鼠模型的建立,损害新生神经元突起生长和新生神经元的存活;有氧训练可改善Aβ25-35损害的大鼠新生神经元突起生长和新生神经元的存活。

引用

页码：255 / 259+275 +275

页数：6

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