Lipopolysaccharide induces neuroglia activation and NF-κB activation in cerebral cortex of adult mice
10.1186/s42826-019-0018-9
- Author:
Ju Bin KANG
1
;
Dong Ju PARK
;
Murad Ali SHAH
;
Myeong Ok KIM
;
Phil Ok KOH
Author Information
1. Department of Anatomy, College of Veterinary Medicine, Research Institute of Life Science, 501 Jinju-daero, Jinju 52828, South Korea. pokoh@gnu.ac.kr
- Publication Type:Original Article
- Keywords:
Lipopolysaccharide;
Neuroinflammation;
Nuclear factor kappa B;
Oxidative stress;
Reactive oxygen species
- MeSH:
Adult;
Animals;
Astrocytes;
Body Weight;
Cerebral Cortex;
Cytokines;
Glial Fibrillary Acidic Protein;
Humans;
Injections, Intraperitoneal;
Male;
Mice;
Microglia;
Necrosis;
Neuroglia;
NF-kappa B;
Oxidative Stress;
Reactive Oxygen Species
- From:Laboratory Animal Research
2019;35(3):132-139
- CountryRepublic of Korea
- Language:English
-
Abstract:
Lipopolysaccharide (LPS) acts as an endotoxin, releases inflammatory cytokines, and promotes an inflammatory response in various tissues. This study investigated whether LPS modulates neuroglia activation and nuclear factor kappa B (NF-κB)-mediated inflammatory factors in the cerebral cortex. Adult male mice were divided into control animals and LPS-treated animals. The mice received LPS (250 µg/kg) or vehicle via an intraperitoneal injection for 5 days. We confirmed a reduction of body weight in LPS-treated animals and observed severe histopathological changes in the cerebral cortex. Moreover, we elucidated increases of reactive oxygen species and oxidative stress levels in LPS-treated animals. LPS administration led to increases of ionized calcium-binding adaptor molecule-1 (Iba-1) and glial fibrillary acidic protein (GFAP) expression. Iba-1 and GFAP are well accepted as markers of activated microglia and astrocytes, respectively. Moreover, LPS exposure induced increases of NF-κB and pro-inflammatory factors, such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Increases of these inflammatory mediators by LPS exposure indicate that LPS leads to inflammatory responses and tissue damage. These results demonstrated that LPS activates neuroglial cells and increases NF-κB-mediated inflammatory factors in the cerebral cortex. Thus, these findings suggest that LPS induces neurotoxicity by increasing oxidative stress and activating neuroglia and inflammatory factors in the cerebral cortex.
