设为首页 电子邮箱 联系我们

本刊最新招聘信息请见“通知公告”!  本刊投稿系统试运行中,欢迎投稿!如投稿有问题,可直接将稿件发送至zgyy8888@163.com

 

主管单位:中华人民共和国   

国家卫生健康委员会

主办单位:
总编辑:
杨秋

编辑部主任:吴翔宇

邮发代号:80-528
定价:28.00元
全年:336.00元
Email:zgyy8888@163.com
电话(传真):010-64428528;
010-64456116(总编室)

                  

2022 年第 1 期 第 17 卷

阿里红多糖干预对β淀粉样蛋白1-42诱导的阿尔茨海默病大鼠脑内氧化应激状态及记忆功能的影响

Effects of Fomes officinalis polysaccharides on cerebral oxidative stress state and memory function in rats with Alzheimer′s disease induced by amyloid β1-42

作者:杨倩邓明珠

英文作者:Yang Qian Deng Mingzhu

单位:湖南省脑科医院神经内二科,长沙410007

英文单位:The Second Department of Neurology Hunan Brain Hospital Changsha 410007 China

关键词:阿尔茨海默病;阿里红多糖;氧化应激;记忆功能

英文关键词:Alzheimer′sdisease;Fomesofficinalispolysaccharides;Oxidativestress;Memoryfunction

  • 摘要:
  • 目的 探讨阿里红多糖干预对β淀粉样蛋白(Aβ)1-42诱导的阿尔茨海默病(AD)大鼠脑内氧化应激状态及记忆功能的影响。方法 60只健康雄性SD大鼠按随机数字表法分为正常对照组、模型对照组、低剂量组、中剂量组、高剂量组、阳性药组,各10只。除正常对照组外,其余各组均使用Aβ1-42诱导建立AD大鼠模型。低剂量组、中剂量组、高剂量组大鼠每日上午分别予以2550100 mg/kg阿里红多糖灌药,阳性药组大鼠每日上午予以0.5 mg/kg盐酸多奈哌齐灌药,正常对照组、模型对照组则每日予以等量蒸馏水灌服,各组均连续灌服30 d。于各组大鼠给药结束24 h后进行Morris水迷宫实验,记录大鼠逃避潜伏期、首次跨越时间和穿越平台次数。检测大鼠海马组织中超氧化物歧化酶(SOD)、丙二醛、活性氧自由基(ROS)、3-硝基酪氨酸(3-NT)、4-羟基壬烯醛(4-HNE)及8-羟基脱氧鸟苷(8-OHdG)水平。结果 模型对照组大鼠第15天的逃避潜伏期、首次跨越时间均显著长于正常对照组,海马组织中SOD水平显著低于正常对照组,而丙二醛、ROS3-NT4-HNE8-OHdG水平均显著高于正常对照组(均P0.05)。低剂量组大鼠上述指标与模型对照组比较,差异均无统计学意义(均P0.05)。而中、高剂量组及阳性药组大鼠第15天的逃避潜伏期、首次跨越时间和海马组织中丙二醛、ROS3-NT4-HNE8-OHdG水平均明显短于/低于模型对照组,穿越平台次数、海马组织中SOD水平均明显多于/高于模型对照组[(5.9±1.5)、(6.8±1.6)、(7.6±1.8)次比(3.2±1.0)次;(115±8)、(132±8)、(141±7kIU/L比(82±7kIU/L](均P0.05)。结论  阿里红多糖能有效改善AD大鼠的记忆功能,其机制可能与减少氧自由基的损伤、加速体内自由基清除,减轻脑内氧化应激损伤有关。

  • Objective   To explore the effects of Fomes officinalis polysaccharides (FOPS) on cerebral oxidative stress state and memory function in rats with Alzheimers disease (AD) induced by amyloid β1-42 (Aβ1-42). Methods  According to random number table method, 60 healthy male SD rats were divided into normal control group, model control group, low-dose group, medium-dose group, high-dose group and positive drug group, with 10 rats in each group. Except for normal control group, rats in other groups were induced by Aβ1-42 to construct AD rat models. Rats in low-dose group, medium-dose group and high-dose group were given 25, 50 and 100 mg/kg FOPS by intragastric administration every morning, rats in positive drug group were given 0.5 mg/kg donepezil hydrochloride every morning, rats in normal control group and model control group were given the same amount of distilled water every morning, and each group was perfused continuously for 30 d. At 24 h after the end of administration, Morris water maze was conducted to record the escape latency, the first crossing time and times of crossing platform. The levels of superoxide dismutase (SOD), malondialdehyde (MDA), reactive oxygen species (ROS), 3-nitrotyrosine (3-NT), 4-hydroxynonenal (4-HNE) and 8-hydroxy-2 deoxyguanosine (8-OHdG) in hippocampus were detected. Results  The escape latency on the 1st to 5th day and the first crossing time in model control group were significantly longer than those in normal control group, the level of SOD of hippocampus was significantly lower than that in normal control group, while levels of MDA, ROS, 3-NT, 4-HNE and 8-OHdG were significantly higher than those in normal control group (all P0.05). The difference in the above indexes between low-dose group and model control group were not statistically significant (all P0.05). Compared with model control group, escape latency on the 1st to 5th day, the first crossing time, and levels of MDA, ROS, 3-NT, 4-HNE and 8-OHdG of hippocampus significantly decreased in middle-dose, high-dose groups and positive drug group, while times of crossing platform and SOD level significantly increased[(5.9±1.5,6.8±1.6,7.6±1.8 times vs 3.2±1.0times;(115±8, 132±8, 141±7kIU/L vs 82±7kIU/L(all P0.05). Conclusions  FOPS can effectively improve memory function of AD rats. The mechanism may be related to reduce ROS damage, accelerate the elimination of radicals and alleviate cerebral oxidative stress damage.

copyright
地址:北京市朝阳区安贞路2号首都医科大学附属北京安贞医院北楼二层
电话:010-64456116 传真:010-64428528 邮编:100029 Email: zgyy8888@163.com
网址: 京ICP备2020043099号-3

当您在使用本网站投稿遇到困难时,请直接将稿件投送到编辑部邮箱zgyy8888@163.com。







安卓


苹果

关闭
Baidu
map