Neuroinflammation induced by lipopolysaccharide causes cognitive impairment in mice
| Autor: | Yong-Mei Fu, Wei Bi, Xiaofeng Cheng, Shu Xiao, Xin Lan, Hongmei Li, Jiayi Zhao, Daxiang Lu, Wei Wei, Jiawei Zhang, Yanping Wang, Lihong Zhu |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Předmět: |
Lipopolysaccharides
Male 0301 basic medicine Lipopolysaccharide Nitric Oxide Synthase Type II Morris water navigation task lcsh:Medicine Pharmacology Nitric Oxide Article Dinoprostone Nitric oxide Mice 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Western blot medicine Animals Cognitive Dysfunction Maze Learning lcsh:Science Neuroinflammation Inflammation Multidisciplinary biology Microglia medicine.diagnostic_test Tumor Necrosis Factor-alpha Chemistry Interleukins lcsh:R NF-kappa B Brain Mice Inbred C57BL Toll-Like Receptor 4 Nitric oxide synthase 030104 developmental biology medicine.anatomical_structure Cyclooxygenase 2 biology.protein Tumor necrosis factor alpha lcsh:Q 030217 neurology & neurosurgery |
| Zdroj: | Scientific Reports, Vol 9, Iss 1, Pp 1-12 (2019) Scientific Reports |
| ISSN: | 2045-2322 |
| DOI: | 10.1038/s41598-019-42286-8 |
| Popis: | In this study, we investigated lipopolysaccharide (LPS)-induced cognitive impairment and neuroinflammation in C57BL/6J mice by using behavioral tests, immunofluorescence, enzyme-linked immunosorbent assay (ELISA) and Western blot. We found that LPS treatment leads to sickness behavior and cognitive impairment in mice as shown in the Morris water maze and passive avoidance test, and these effects were accompanied by microglia activation (labeled by ionized calcium binding adaptor molecule-1, IBA-1) and neuronal cell loss (labeled by microtubule-associated protein 2, MAP-2) in the hippocampus. The levels of interleukin-4 (IL-4) and interleukin-10 (IL-10) in the serum and brain homogenates were reduced by the LPS treatment, while the levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), prostaglandin E2 (PGE2) and nitric oxide (NO) were increased. In addition, LPS promoted the expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) in the brain homogenates. The Western blot analysis showed that the nuclear factor kappa B (NF-κB) signaling pathway was activated in the LPS groups. Furthermore, VIPER, which is a TLR-4-specific inhibitory peptide, prevented the LPS-induced neuroinflammation and cognitive impairment. These data suggest that LPS induced cognitive impairment and neuroinflammation via microglia activation by activating the NF-kB signaling pathway; furthermore, we compared the time points, doses, methods and outcomes of LPS administration between intraperitoneal and intracerebroventricular injections of LPS in LPS-induced neuroinflammation and cognitive impairment, and these data may provide additional insight for researchers performing neuroinflammation research. |
| Databáze: | OpenAIRE |
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