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富氢盐水通过抑制 JNK 和 NF-κB 的激活减轻氧化应激和炎症反应,在淀粉样β诱导的阿尔茨海默病大鼠模型中。

Hydrogen-rich saline reduces oxidative stress and inflammation by inhibit of JNK and NF-κB activation in a rat model of amyloid-beta-induced Alzheimer's disease.

机构信息

Department of Neurology, the First Affiliated Hospital of China Medical University, Shenyang 110001, PR China.

出版信息

Neurosci Lett. 2011 Mar 17;491(2):127-32. doi: 10.1016/j.neulet.2011.01.022. Epub 2011 Jan 14.

DOI:10.1016/j.neulet.2011.01.022
PMID:21238541
Abstract

This study is to examine if hydrogen-rich saline reduced amyloid-beta (Aβ) induced neural inflammation and oxidative stress in a rat model by attenuation of activation of JNK and NF-κB. Sprague-Dawley male rats (n=18, 280-330 g) were divided into three groups, sham operated, Aβ1-42 injected and Aβ1-42 plus hydrogen-rich saline treated animals. Hydrogen-rich saline (5 ml/kg, i.p., daily) was injected for 10 days after intraventricular injection of Aβ1-42. The levels of IL-1β were assessed by ELISA analysis, 8-OH-dG by immunohistochemistry in the brain slides, and JNK and NF-κB by immunohistochemistry and western blotting. After Aβ1-42 injection, the level of IL-1β, 8-OH-dG, JNK and NF-κB all increased in brain tissues, while hydrogen-rich saline treatment decreased the level of IL-1β, 8-OH-dG and the activation of JNK and NF-κB. In conclusion, hydrogen-rich saline prevented Aβ-induced neuroinflammation and oxidative stress, possibly by attenuation of activation of c-Jun NH₂-terminal kinase (JNK) and nuclear factor-κB (NF-κB) in this rat model.

摘要

本研究旨在通过抑制 JNK 和 NF-κB 的激活,来观察富氢盐水是否能减轻 Aβ 诱导的神经炎症和氧化应激。雄性 Sprague-Dawley 大鼠(n=18,体重 280-330g)分为三组:假手术组、Aβ1-42 注射组和 Aβ1-42 加富氢盐水处理组。在脑室注射 Aβ1-42 后,每天腹腔注射 5ml/kg 的富氢盐水 10 天。通过 ELISA 分析检测脑内 IL-1β 水平,通过免疫组化检测脑切片中的 8-OH-dG,通过免疫组化和 Western blot 检测 JNK 和 NF-κB。在 Aβ1-42 注射后,大鼠脑组织中 IL-1β、8-OH-dG、JNK 和 NF-κB 的水平均升高,而富氢盐水处理则降低了 IL-1β、8-OH-dG 和 JNK 和 NF-κB 的激活水平。综上所述,富氢盐水可能通过抑制 c-Jun NH₂-末端激酶(JNK)和核因子-κB(NF-κB)的激活,预防 Aβ 诱导的神经炎症和氧化应激。

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