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脂多糖诱导脓毒症大鼠脑内氧化损伤及相关信号通路的研究

陈锋 刘英富 李光宗 张益 郁硕 樊毫军 侯世科

军事医学2016,Vol.40Issue(9):703-706,4.
军事医学2016,Vol.40Issue(9):703-706,4.DOI:10.7644/j.issn.1674-9960.2016.09.002

脂多糖诱导脓毒症大鼠脑内氧化损伤及相关信号通路的研究

Oxidative damage and related signal pathways caused by lipopolysaccharide induced sepsis in rat brain

陈锋 1刘英富 2李光宗 3张益 3郁硕 3樊毫军 3侯世科3

作者信息

  • 1. 天津医科大学研究生院,天津 300070
  • 2. 武警后勤学院附属医院救援医学研究所,天津 300162
  • 3. 武警后勤学院附属医院救援医学研究所,天津 300162
  • 折叠

摘要

Abstract

Objective To investigate the mechanism of oxidative damage caused by lipopolysaccharide (LPS)induced sepsis in rat brain.Methods The rats were randomly divided into control group and model group (low LPS group and high LPS group).Twenty-four hours after the modeling,the rats were sacrificed before their brain tissue was taken out and prepared for the test.The changes in malondialdehyde (MDA),superoxide dismutase (SOD),glutathione peroxidase (GSH-Px),total antioxidant capacity (T-AOC),hydrogen peroxide (H2 O2 )and succinate dehydrogenase (SDH)were detected.The expression level of JNK and Nrf2 protein in brain tissue was detected by qRT-PCR and Western blotting. Results Compared with the control group,the MDA,SOD,GSH-px,T-AOC,H2O2 and SDH level increased significantly in the model group,and the difference in expressions of JNK and Nrf2 was statistically significant (P <0.05). Conclusion The LPS induced septic oxidative brain damage model in rats is successfully established,and the process may be regulated through the Nrf2 and JNK signal pathways.

关键词

脂多糖类/脓毒症/脑损伤/丙二醛/超氧化物歧化酶/过氧化氢/琥珀酸脱氢酶

Key words

lipopolysaccharides/sepsis/brain injuries/malondialdehyde/superoxide dismutase/hydrogen peroxide/succinate dehydro genase

分类

医药卫生

引用本文复制引用

陈锋,刘英富,李光宗,张益,郁硕,樊毫军,侯世科..脂多糖诱导脓毒症大鼠脑内氧化损伤及相关信号通路的研究[J].军事医学,2016,40(9):703-706,4.

基金项目

天津市科技计划资助项目(14ZCDZSY00033);天津市应用基础与前沿技术研究计划资助项目(14JCQNJC12600);全军重点实验室开放基金资助项目 ()

军事医学

OA北大核心CSCDCSTPCD

1674-9960

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