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宫内感染致脑损伤对仔鼠认知发育和海马神经发生的影响
引用本文:江佩芳,朱涛,杨翠微,高峰,顾伟忠,袁天明,俞惠民.宫内感染致脑损伤对仔鼠认知发育和海马神经发生的影响[J].中国病理生理杂志,2014,30(11):1934-1940.
作者姓名:江佩芳  朱涛  杨翠微  高峰  顾伟忠  袁天明  俞惠民
作者单位:1浙江大学医学院附属儿童医院神经内科,浙江 杭州 310003; 2浙江大学医学院附属邵逸夫医院ICU,浙江 杭州 310016
基金项目:国家自然科学基金资助项目(No. 81201511);浙江省医药卫生科技计划(No. 2010KYB064);浙江省教育厅科研项目(No. Y201225805);浙江省人口计生委科研项目(No. JSW2012-A011)
摘    要: 目的:探讨宫内感染致仔鼠脑损伤后对认知发育和海马神经发生的影响。方法: 15只Sprague-Dawley孕鼠(孕15 d)按随机数字表法分为造模组(8只)和对照组(7只)。繁殖后的2组雄性仔鼠按随机数字表法分为宫内感染组(35只)和对照组(35只),进行大脑解剖学观察、神经细胞凋亡检测、Morris水迷宫实验、神经细胞增殖及存活分析。结果: (1)宫内感染组仔鼠大脑较对照组萎缩,TUNEL阳性细胞数和caspase-3阳性细胞数均较对照组显著增加 (P<0.05)。(2)宫内感染组仔鼠近期记忆及远期记忆保持能力均较对照组降低,潜伏期显著延长(P<0.05)。(3)细胞增殖分析显示宫内感染组3 、7 和14日龄仔鼠BrdU阳性细胞数较对照组显著增加(P<0.05);细胞存活分析显示,28日龄的2组仔鼠BrdU阳性细胞数无显著差异(P>0.05)。结论: 宫内感染可致仔鼠脑损伤,海马神经细胞凋亡可能与认知发育障碍密切相关。宫内感染诱导的神经发生可能与脑损伤后神经自身修复有关。

关 键 词:宫内感染  脑损伤  神经细胞凋亡  认知发育  神经发生  
收稿时间:2014-06-19

Brain injury induced by intrauterine infection affects offspring’s cognitive development and hippocampal neurogenesis
JIANG Pei-fang,ZHU Tao,YANG Cui-wei,GAO Feng,GU Wei-zhong,YUAN Tian-ming,YU Hui-min.Brain injury induced by intrauterine infection affects offspring’s cognitive development and hippocampal neurogenesis[J].Chinese Journal of Pathophysiology,2014,30(11):1934-1940.
Authors:JIANG Pei-fang  ZHU Tao  YANG Cui-wei  GAO Feng  GU Wei-zhong  YUAN Tian-ming  YU Hui-min
Institution:1Department of Neurology, Children’s Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China; 2Department of Critical Care Medicine, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou 310016, China.
Abstract:AIM: To explore the effect of brain injury induced by intrauterine infection on offspring’s cognitive development and hippocampal neurogenesis. METHODS: Sprague-Dawley pregnant rats (n=15) were randomly divided into model group (n=8) and control group (n=7). After delivery, the male pups were randomly divided into E. coligroup (n=35) and control group (n=35). Total 20 male pups at postnatal day 28 (P28) were randomly divided into 2 groups for Morris water maze test. Hippocampi of the 2 groups were used for cell apoptosis, neuronal proliferation and survival analysis. RESULTS: (1) The brain tissue was slightly atrophied in E. coligroup. The numbers of TUNEL and caspase-3 positive cells were significantly increased in E. coligroup (P<0.05). (2) In the navigation and memory task, the rats in E. coligroup had longer escape latency than that in control group (P<0.05). (3) There was a significant increase in the BrdU-labeled cells at P3, P7 and P14 in E. coligroup than that in control group (P<0.05). When the cells got mature, no significant difference of BrdU-labeled cells at P28 between the 2 groups was observed (P>0.05). CONCLUSION: Intrauterine infection increases hippocampal neuronal apoptosis, which may be regarded as an etiological factor in the cognitive development impairment. Inflammation-induced neurogenesis may play an important role in neuronal protection and repair in immature brain after intrauterine infection.
Keywords:Intrauterine infection  Brain injury  Neuronal apoptosis  Cognitive development  Neurogenesis
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