史云洁,王鑫,王沛,马姗婕,朱婧,常静一,陈希民,何梅.叶黄素对老年痴呆小鼠学习记忆能力的改善作用[J].中国食品卫生杂志,2016,28(6):703-708. 本文二维码信息
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叶黄素对老年痴呆小鼠学习记忆能力的改善作用
Effect of lutein intervention on cognitive competence in SAMP8
投稿时间:2016-10-27  
DOI:
中文关键词:  叶黄素  老年痴呆  快速老化痴呆模型小鼠(SAMP8)  抗氧化  学习记忆  Morris水迷宫  机制
Key Words:Lutein  Alzheimer's disease  senescence-accelerated mouse prone 8 (SAMP8)  antioxidant  cognitive competence  Morris water maze  mechanism
基金项目:国家科技支撑计划课题(2012BAD33B01);北京市科学技术研究院海外人才专项资助项目(OTP-2014-001);北京市科学技术研究院创新团队计划(IG201407C2)
作者单位E-mail
史云洁 北京市营养源研究所,北京 100069 yunjie_s@126.com,hemei2003@163.com 
王鑫 北京中科邦尼国际科技有限责任公司,北京 100069  
王沛 北京中科邦尼国际科技有限责任公司,北京 100069  
马姗婕 北京中科邦尼国际科技有限责任公司,北京 100069  
朱婧 北京市营养源研究所,北京 100069  
常静一 北京中科邦尼国际科技有限责任公司,北京 100069  
陈希民 北京中科邦尼国际科技有限责任公司,北京 100069  
何梅 北京市营养源研究所,北京 100069 yunjie_s@126.com,hemei2003@163.com 
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中文摘要:
      探讨叶黄素对老年痴呆(AD)模型小鼠学习记忆能力的影响及相关作用机制。方法 采用5月龄雄性快速老化痴呆模型小鼠(SAMP8)作为自然发病的AD模型,随机分为AD模型组和3个叶黄素剂量组(15、30、60 mg/kg BW),采用正常老化小鼠(SAMR1)作为正常对照组,连续灌胃8周。灌胃结束后采用Morris水迷宫对小鼠进行学习记忆能力测验,取小鼠脑组织检测超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽(GSH)、丙二醛(MDA)和乙酰胆碱酯酶(AchE)水平,取小鼠海马组织进行病理学观察。结果 与AD模型组比较,叶黄素中、高剂量组的潜伏期明显缩短,差异有统计学意义(P<0.05);3个叶黄素剂量组的CAT、AchE活性均明显升高,GSH含量明显增加,MDA含量明显降低,差异均有统计学意义(P<0.05);叶黄素高剂量组海马组织细胞异常明显减少。结论 叶黄素可改善快速老化痴呆模型小鼠的学习记忆能力,其作用机制之一可能是提升小鼠的抗氧化能力,减少氧化应激损伤。
Abstract:
      To investigate the effect of lutein intervention on cognitive competence in mice with Alzheimer's disease (AD) and the related mechanism.Methods Use 5-month male senescence-accelerated mouse prone 8 (SAMP8) as a natural model of AD. SAMP8s were randomly assigned into 1 AD model group and 3 lutein intervention groups; senescence-accelerated mouse resistant 1(SAMR1) were used as control.15,0, 60 mg/kg BW lutein was given to the 3 intervention groups, once a day via intragastric administration for 8 weeks. Cognitive competence was assessed by the Morris water maze after intervention. Levels of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), malondialdehyde (MDA) and acetylcholinesterase (AchE) in brain tissue were measured. The pathological observation of the hippocampus was performed. Results Medium and high level of lutein intervention lowered the escape latency SAMP8(P<0.05). Lutein intervention increased the levels of CAT, GSH, AchE and lowered MDA(P<0.05). High level lutein reduced the number of abnormal cells in hippocampus(P<0.05).Conclusion Lutein can improve the cognitive competence of SAMP8 and one of its possible mechanisms was by enhancing oxidation resistance and reducing oxidative damage.
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