Oxidative damage and related signal pathways caused by lipopolysaccharide induced sepsis in rat brain
10.7644/j.issn.1674-9960.2016.09.002
- VernacularTitle: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
- Author:
Feng CHEN
;
Yingfu LIU
;
Guangzong LI
;
Yi ZHANG
;
Shuo YU
;
Haojun FAN
;
Shike HOU
- Publication Type:Journal Article
- Keywords:
lipopolysaccharides;
sepsis;
brain injuries;
malondialdehyde;
superoxide dismutase;
hydrogen peroxide;
succinate dehydro genase
- From:
Military Medical Sciences
2016;40(9):703-706
- CountryChina
- Language:Chinese
-
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.
