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- Title
Oxytocin inhibits lipopolysaccharide-induced inflammation in microglial cells and attenuates microglial activation in lipopolysaccharide-treated mice.
- Authors
Lin Yuan; Song Liu; Xuemei Bai; Yan Gao; Guangheng Liu; Xueer Wang; Dexiang Liu; Tong Li; Aijun Hao; Zhen Wang; Yuan, Lin; Liu, Song; Bai, Xuemei; Gao, Yan; Liu, Guangheng; Wang, Xueer; Liu, Dexiang; Li, Tong; Hao, Aijun; Wang, Zhen
- Abstract
<bold>Background: </bold>Overactivated microglia is involved in various kinds of neurodegenerative diseases. Suppression of microglial overactivation has emerged as a novel strategy for treatment of neuroinflammation-based neurodegeneration. In the current study, anti-inflammatory effects of oxytocin (OT), which is a highly conserved nonapeptide with hormone and neurotransmitter properties, were investigated in vitro and in vivo.<bold>Methods: </bold>BV-2 cells and primary microglia were pre-treated with OT (0.1, 1, and 10 μM) for 2 h followed by LPS treatment (500 ng/ml); microglial activation and pro-inflammatory mediators were measured by Western blot, RT-PCR, and immunofluorescence. The MAPK and NF-κB pathway proteins were assessed by Western blot. The intracellular calcium concentration ([Ca(2+)]i) was determined using Fluo2-/AM assay. Intranasal application of OT was pre-treated in BALB/C mice (adult male) followed by injected intraperitoneally with LPS (5 mg/kg). The effect of OT on LPS-induced microglial activation and pro-inflammatory mediators was measured by Western blot, RT-PCR, and immunofluorescence in vivo.<bold>Results: </bold>Using the BV-2 microglial cell line and primary microglia, we found that OT pre-treatment significantly inhibited LPS-induced microglial activation and reduced subsequent release of pro-inflammatory factors. In addition, OT inhibited phosphorylation of ERK and p38 but not JNK MAPK in LPS-induced microglia. OT remarkably reduced the elevation of [Ca(2+)]i in LPS-stimulated BV-2 cells. Furthermore, a systemic LPS-treated acute inflammation murine brain model was used to study the suppressive effects of OT against neuroinflammation in vivo. We found that pre-treatment with OT showed marked attenuation of microglial activation and pro-inflammatory factor levels.<bold>Conclusions: </bold>Taken together, the present study demonstrated that OT possesses anti-neuroinflammatory activity and might serve as a potential therapeutic agent for treating neuroinflammatory diseases.
- Subjects
MICROGLIA; NEURODEGENERATION; INFLAMMATION; PEPTIDES; NEUROTRANSMITTERS; ANIMAL models in research; CELL metabolism; BRAIN metabolism; ANIMAL experimentation; ANTI-inflammatory agents; BRAIN; CELLS; COMPARATIVE studies; FLUORESCENT antibody technique; RESEARCH methodology; MEDICAL cooperation; MICE; OXYTOCIN; POLYMERASE chain reaction; RESEARCH; WESTERN immunoblotting; EVALUATION research; REVERSE transcriptase polymerase chain reaction; LIPOPOLYSACCHARIDES; PHARMACODYNAMICS
- Publication
Journal of Neuroinflammation, 2016, Vol 13, p1
- ISSN
1742-2094
- Publication type
journal article
- DOI
10.1186/s12974-016-0541-7