Extract of Fructus Schisandrae chinensis Inhibits Neuroinflammation Mediator Production from Microglia via NF-κ B and MAPK Pathways.
10.1007/s11655-018-3001-7
- Author:
Fang-Jiao SONG
1
;
Ke-Wu ZENG
2
;
Jin-Feng CHEN
2
;
Yuan LI
1
;
Xiao-Min SONG
2
;
Peng-Fei TU
2
;
Xue-Mei WANG
3
Author Information
1. Research Studio of Integration of Traditional and Western Medicine, First Hospital, Peking University, Beijing, 100034, China.
2. State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, Beijing, 100191, China.
3. Research Studio of Integration of Traditional and Western Medicine, First Hospital, Peking University, Beijing, 100034, China. wangxuemeibjmu@163.com.
- Publication Type:Journal Article
- Keywords:
Fructus Schisandrae chinensis;
microglia;
mitogenactivated protein kinase;
neuroinflammation;
nuclear factor-κ B
- MeSH:
Animals;
Astrocytes;
drug effects;
metabolism;
pathology;
Cell Line;
Cell Nucleus;
drug effects;
metabolism;
Chromatography, High Pressure Liquid;
Down-Regulation;
drug effects;
Inflammation;
pathology;
Inflammation Mediators;
metabolism;
Lipopolysaccharides;
MAP Kinase Signaling System;
drug effects;
Mice, Inbred ICR;
Microglia;
drug effects;
metabolism;
pathology;
NF-kappa B;
metabolism;
Nervous System;
pathology;
Neurons;
drug effects;
metabolism;
pathology;
Neuroprotective Agents;
pharmacology;
Plant Extracts;
pharmacology;
Schisandra;
chemistry;
Spectrometry, Mass, Electrospray Ionization
- From:
Chinese journal of integrative medicine
2019;25(2):131-138
- CountryChina
- Language:English
-
Abstract:
OBJECTIVE:To investigate the anti-neuroinflammation effect of extract of Fructus Schisandrae chinensis (EFSC) on lipopolysaccharide (LPS)-induced BV-2 cells and the possible involved mechanisms.
METHODS:Primary cortical neurons were isolated from embryonic (E17-18) cortices of Institute of Cancer Research (ICR) mouse fetuses. Primary microglia and astroglia were isolated from the frontal cortices of newborn ICR mouse. Different cells were cultured in specific culture medium. Cells were divided into 5 groups: control group, LPS group (treated with 1 μg/mL LPS only) and EFSC groups (treated with 1 μg/mL LPS and 100, 200 or 400 mg/mL EFSC, respectively). The effect of EFSC on cells viability was tested by methylthiazolyldiphenyltetrazolium bromide (MTT) colorimetric assay. EFSC-mediated inhibition of LPS-induced production of pro-inflammatory mediators, such as nitrite oxide (NO) and interleukin-6 (IL-6) were quantified and neuron-protection effect against microglia-mediated inflammation injury was tested by hoechst 33258 apoptosis assay and crystal violet staining assay. The expression of pro-inflammatory marker proteins was evaluated by Western blot analysis or immunofluorescence.
RESULTS:EFSC (200 and 400 mg/mL) reduced NO, IL-6, inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) expression in LPS-induced BV-2 cells (P<0.01 or P<0.05). EFSC (200 and 400 mg/mL) reduced the expression of NO in LPS-induced primary microglia and astroglia (P<0.01). In addition, EFSC alleviated cell apoptosis and inflammation injury in neurons exposed to microglia-conditioned medium (P<0.01). The mechanistic studies indicated EFSC could suppress nuclear factor (NF)-?B phosphorylation and its nuclear translocation (P<0.01). The anti-inflammatory effect of EFSC occurred through suppressed activation of mitogen-activated protein kinase (MAPK) pathway (P<0.01 or P<0.05).
CONCLUSION:EFSC acted as an anti-inflammatory agent in LPS-induced glia cells. These effects might be realized through blocking of NF-κB activity and inhibition of MAPK signaling pathways.
