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CaMKII反义寡核苷酸对阿尔茨海默病样大鼠海马细胞损伤的保护作用及其机制

赵小芳 钱冰 王静 吕春娥 宋远见 刘志安

西安交通大学学报(医学版)2017,Vol.38Issue(1):13-17,5.
西安交通大学学报(医学版)2017,Vol.38Issue(1):13-17,5.DOI:10.7652/jdyxb201701003

CaMKII反义寡核苷酸对阿尔茨海默病样大鼠海马细胞损伤的保护作用及其机制

Protective effects of CaMKII antisense oligonucleotide on cell inj ury of rat hippocampus induced by Alzheimer’s disease and its mechanism

赵小芳 1钱冰 2王静 1吕春娥 3宋远见 4刘志安1

作者信息

  • 1. 徐州医科大学解剖学教研室,江苏徐州 221004
  • 2. 杭州师范大学医学院,浙江杭州 311121
  • 3. 徐州卫生学校,江苏徐州 221400
  • 4. 徐州医科大学遗传学教研室,江苏徐州 221004
  • 折叠

摘要

Abstract

ABSTRACT:Objective To study the protective effects of CaMKII antisense oligonucleotide on cell injury of rat hippocampus induced by Alzheimer’s disease (AD ) and its mechanism.Methods AD-like rat model was established by Aβ1-40 and AlCl3 intervention method.The model rats were then randomly divided into AD model group (AD),solvent control group (TE),CaMKII antisense oligonucleotide group (AS),and CaMKII missense oligonucleotide group (MS).The escape latency of the rats was observed by Morris water maze;the damage of hippocampal cells was detected by HE staining and TUNEL staining.The changes of CaMKII,NR1 and NR2B expressions in rat hippocampus were detected by Western blot.Results Compared with those in AD group,TE group and MS group the escape latency of rats was significantly shorter, the hippocampal neurons damage significantly reduced and CaMKII,NR1 and NR2B protein expressions were significantly decreased in CaMKII antisense oligonucleotide group (P<0.05).Conclusion CaMKII antisense oligonucleotide plays a neuroprotective role by reducing the AD-like rat hippocampus cell damage and improve learning and memory ability,which may be related to the pathologically high expressions of CaMKII,NR1 and NR2B.

关键词

CaMKII/NR1/NR2B/阿尔茨海默病/大鼠/海马

Key words

CaMKII/NR1/NR2B/Alzheimer’s disease/rat/hippocampus

分类

医药卫生

引用本文复制引用

赵小芳,钱冰,王静,吕春娥,宋远见,刘志安..CaMKII反义寡核苷酸对阿尔茨海默病样大鼠海马细胞损伤的保护作用及其机制[J].西安交通大学学报(医学版),2017,38(1):13-17,5.

基金项目

国家自然科学基金资助项目(No.81371300) (No.81371300)

徐州医科大学校长专项人才基金资助项目(No.2012KJZ08) Supported by the National Natural Science Foundation of China (No.81371300)and Xuzhou Medical University President Fund of Special Talents (No.2012KJZ08) (No.2012KJZ08)

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