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作 者:韩敏敏 郝翠[1,2] 王喆 许杰 张丽娟[1,2] 郭云良[1] 徐涛[1,3] HAN Min-min;HAO Cui;WANG Zhe;XU Jie;ZHANG Li-juan;GUO Yun-liang;XU Tao(Institute of Integrative Medicine,Qingdao University,Qingdao 266021,China;Systems Biology & Medicine Center for Complex Diseases,Affiliated Hospital of Qingdao University,Qingdao 266003,China;Department of traditional Chinese medicine,Qingdao Women and Children's Hospital,Qingdao 266034,China)
机构地区:[1]青岛大学中西医结合中心,山东青岛266021 [2]青岛大学附属医院系统生物医学研究中心,山东青岛266003 [3]青岛市妇女儿童医院中医科,山东青岛266034
出 处:《中国海洋药物》2018年第4期39-44,共6页Chinese Journal of Marine Drugs
基 金:国家自然科学基金项目(31500646);山东省自然科学基金项目(BS2015YY040);青岛市科技发展计划项目(15-9-1-67-JCH);山东省中医药局发展计划项目(2015-183)资助
摘 要:目的研究虾青素对β-淀粉样蛋白(Aβ)诱导的损伤模拟阿尔茨海默病(AD)模型大鼠学习记忆功能的改善作用,并探讨其作用机制。方法按随机数字表法将大鼠随机分为假手术组(Control),模型组(Aβ),虾青素组(AXT)。模型组、虾青素组采用侧脑室定位注射Aβ25-35建立AD动物模型。造模后第8天开始灌胃,假手术组、模型组给予玉米油5mL/(kg·d),虾青素组按照25 mg/(kg·d)灌胃,连续灌胃给药21d后进行Morris水迷宫实验,检测大鼠的学习记忆能力;采用ELISA法检测大鼠海马组织中超氧化物歧化酶(SOD)、乳酸脱氢酶(LDH)及丙二醛(MDA)含量以及磷酸化Tau蛋白含量,数据采用单因素方差分析。结果与模型组相比,虾青素组能明显缩短大鼠逃避潜伏期的时间,增加其穿越平台的次数,显著提高大鼠海马组织的SOD含量,降低LDH和MDA含量从而减轻AD大鼠氧化应激状态,降低磷酸化Tau蛋白水平。结论虾青素能通过提高AD大鼠海马组织的抗氧化能力和降低磷酸化Tau蛋白含量,从而改善AD大鼠的学习记忆能力,对Aβ25-35所致的阿尔茨海默病症有一定的治疗效果。Objective To investigate the improvement effects and mechanisms of astaxanthin on the learning and memory function of Alzheimer’s disease model rats induced by Aβ.Methods SD rats were randomly divided into 3 groups,including sham operation group[Control,5 mL/(kg·d)corn oil],model group[Aβ,5 mL/(kg·d)corn oil]and astaxanthin group[AXT,25 mg/(kg·d)astaxanthin].In the model group and astaxanthin group,the rats were injected with Aβ25-35 into the lateral ventricle.After a treatment period of 21 days,the Morris water maze test was carried out to detect the learning and memory ability of rats.The contents of superoxide dismutase(SOD),lactate dehydrogenase(LDH),malondialdehyde(MDA)and phosphorylated Tau(p-Tau)protein in the hippocampus of rats were determined by ELISA assay.All data was analyzed by one-way ANOVA.Results Compared with the model group,astaxanthin group could significantly shorten the time of escape latency,increase the number of platform crossing,increase the content of SOD in the hippocampus,reduce the content of LDH and MDA,as well as reduce the phosphorylation of Tau protein.Conclusion Astaxanthin could improve the learning and memory function of AD rats through enhancing the anti-oxidation ability and decreasing the content of phosphorylated Tau protein in the hippocampus of AD rats,suggesting that it possessed therapeutic effects on the AD induced by Aβ25-35.
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