Lipopolysaccharide induces neuroglia activation and NF-κB activation in cerebral cortex of adult mice

• Published in: Laboratory animal research 2019, 35(3), , pp.132-139
• Main Authors: Kang, Ju-Bin, Park, Dong-Ju, Shah, Murad-Ali, Kim, Myeong-Ok, Koh, Phil-Ok
• Format: Article
• Language: English
• Subjects: Alcohol; Animals; Antibodies; Apoptosis; Astrocytes; Biotechnology; Body weight; Calcium; Cerebral cortex; Cerebrum; Cytokines; Ethanol; Gene expression; Glia; Glial cells; Glial fibrillary acidic protein; IL-1β; Inflammation; Lipid peroxidation; Lipids; Lipopolysaccharide; Lipopolysaccharides; Membranes; Microglia; Neuroinflammation; Neurotoxicity; NF-κB protein; Nuclear factor kappa B; Oxidative stress; Proteins; Reactive oxygen species; Tumor necrosis factor-TNF; Tumor necrosis factor-α; 수의학
• ISSN: 1738-6055; 2233-7660; 2233-7660
• DOI: 10.1186/s42826-019-0018-9

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.