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

目的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(Ach E)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、Ach E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。

Objective 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. SAMP8 s were randomly assigned into 1 AD model group and 3 lutein intervention groups;senescence-accelerated mouse resistant 1（ SAMR1） were used as control. 15,30,60 mg / kg BW lutein was given to the3 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（ Ach E） 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,Ach E 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.