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富氢盐水通过降低氧化应激改善淀粉样β诱导的阿尔茨海默病大鼠的记忆功能。

Hydrogen-rich saline improves memory function in a rat model of amyloid-beta-induced Alzheimer's disease by reduction of oxidative stress.

机构信息

Department of Neurology, the First Affiliated Hospital of China Medical University, Shengyang, PR China.

出版信息

Brain Res. 2010 Apr 30;1328:152-61. doi: 10.1016/j.brainres.2010.02.046. Epub 2010 Feb 19.

Abstract

This study is to examine if hydrogen-rich saline reduced amyloid beta (Abeta) induced neural inflammation, and learning and memory deficits in a rat model. S-D male rats (n=84, 280-330g) were divided into three groups, sham-operated, Abeta1-42 injected and Abeta1-42 plus hydrogen-rich saline-treated animals. Hydrogen-rich saline (5ml/kg, i.p., daily) was injected for 14days after intracerebroventricular injection of Abeta1-42. The levels of MDA, IL-6 and TNF-alpha were assessed by biochemical and ELISA analysis. Morris Water Maze and open field task were used to assess the memory dysfunction and motor dysfunction, respectively. LTP were used to detect the electrophysiology changes, HNE and GFAP immunohistochemistry were used to assess the oxidative stress and glial cell activation. After Abeta1-42 injection, the levels of MDA, IL-6, and TNF-alpha were increased in brain tissues and hydrogen-rich saline treatment suppressed MDA, IL-6, and TNF-alpha concentration. Hydrogen-rich saline treatment improved Morris Water Maze and enhanced LTP in hippocampus blocked by Abeta1-42. Furthermore, hydrogen-rich saline treatment also decreased the immunoreactivitiy of HNE and GFAP in hippocampus induced by Abeta1-42. In conclusion, hydrogen-rich saline prevented Abeta-induced neuroinflammation and oxidative stress, which may contribute to the improvement of memory dysfunction in this rat model.

摘要

本研究旨在探讨富氢盐水是否能减轻淀粉样蛋白β(Abeta)诱导的神经炎症以及学习记忆障碍。S-D 雄性大鼠(n=84,体重 280-330g)分为三组:假手术组、Abeta1-42 注射组和 Abeta1-42 加富氢盐水处理组。Abeta1-42 脑室注射后,每天腹腔注射富氢盐水(5ml/kg),共 14 天。采用生化和 ELISA 分析评估 MDA、IL-6 和 TNF-α 水平。Morris 水迷宫和旷场实验分别用于评估记忆功能障碍和运动功能障碍。LTP 用于检测电生理变化,HNE 和 GFAP 免疫组化用于评估氧化应激和神经胶质细胞激活。Abeta1-42 注射后,脑组织中 MDA、IL-6 和 TNF-α 水平升高,富氢盐水处理抑制 MDA、IL-6 和 TNF-α 浓度。富氢盐水处理改善了 Morris 水迷宫,增强了被 Abeta1-42 阻断的海马 LTP。此外,富氢盐水处理还降低了 Abeta1-42 诱导的海马中 HNE 和 GFAP 的免疫反应性。总之,富氢盐水可预防 Abeta 诱导的神经炎症和氧化应激,这可能有助于改善该大鼠模型的记忆功能障碍。

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