Oxytocin inhibits lipopolysaccharide-induced inflammation in microglial cells and attenuates microglial activation in lipopolysaccharide-treated mice
Inflammation
Lipopolysaccharides
0301 basic medicine
Mice, Inbred BALB C
Reverse Transcriptase Polymerase Chain Reaction
Research
Immunology
Blotting, Western
Anti-Inflammatory Agents
Brain
Fluorescent Antibody Technique
Oxytocin
3. Good health
Cellular and Molecular Neuroscience
Mice
03 medical and health sciences
Neurology
Animals
Microglia
DOI:
10.1186/s12974-016-0541-7
Publication Date:
2016-04-14T06:43:39Z
AUTHORS (10)
ABSTRACT
Overactivated microglia is involved in various kinds of neurodegenerative diseases. Suppression microglial overactivation has emerged as a novel strategy for treatment neuroinflammation-based neurodegeneration. In the current study, anti-inflammatory effects oxytocin (OT), which highly conserved nonapeptide with hormone and neurotransmitter properties, were investigated vitro vivo. BV-2 cells primary pre-treated OT (0.1, 1, 10 μM) 2 h followed by LPS (500 ng/ml); activation pro-inflammatory mediators measured Western blot, RT-PCR, immunofluorescence. The MAPK NF-κB pathway proteins assessed blot. intracellular calcium concentration ([Ca2+]i) was determined using Fluo2-/AM assay. Intranasal application BALB/C mice (adult male) injected intraperitoneally (5 mg/kg). effect on LPS-induced immunofluorescence Using cell line microglia, we found that pre-treatment significantly inhibited reduced subsequent release factors. addition, phosphorylation ERK p38 but not JNK microglia. remarkably elevation [Ca2+]i LPS-stimulated cells. Furthermore, systemic LPS-treated acute inflammation murine brain model used to study suppressive against neuroinflammation We showed marked attenuation factor levels. Taken together, present demonstrated possesses anti-neuroinflammatory activity might serve potential therapeutic agent treating neuroinflammatory
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