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Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
Published on: January 30, 2014
Inhibitory effect of fucoidan on nitric oxide production in lipopolysaccharide-activated primary microglia
Yan-Qiu Cui1, Li-Juan Zhang, Ting Zhang
1Key Laboratory of Neurodegenerative Diseases of Ministry of Education, Capital Medical University, Beijing, China.
Abstract:
1. Microglial activation plays an important role in the pathogenesis of neurodegenerative diseases by producing various pro-inflammatory cytokines. Microglia-derived nitric oxide (NO) is critical for the lipopolysaccharide (LPS)-induced selective loss of dopaminergic neurons. 2. Fucoidan is a sulphated polysaccharide extracted from brown seaweeds. It has a variety of biological actions, including anticoagulant, antiviral and anti-inflammatory effects. The aim of the present study was to investigate the effects of fucoidan on LPS-induced cellular activation in microglia and to evaluate the inhibitory mechanisms involved. 3. To investigate the effects of fucoidan on LPS-induced cellular activation in microglia, primary microglial cells were preincubated with fucoidan (31.25, 62.5 and 125 microg/mL) for 10 min, followed by stimulation with LPS (0.01 microg/mL). Then, cell shape and NO production were determined 24 h after LPS stimulation, whereas inducible nitric oxide synthase (iNOS) mRNA and protein expression were determined at 6 and 18 h after LPS stimulation, respectively. To evaluate the inhibitory mechanisms involved, mitogen-activated protein kinase (MAPK) activation was also evaluated. 4. Lipopolysaccharide transformed cells into an amoeboid shape, whereas 62.5 microg/mL fucoidan inhibited this activation. Moreover, 125 microg/mL fucoidan significantly inhibited microglial NO production to 75% of that in LPS-treated group and also significantly diminished the expression of iNOS mRNA and protein by nearly 50%. Fucoidan (125 microg/mL) also suppressed phosphorylation of p38 and extracellular signal-regulated kinase (ERK) by approximately 50%, but not that of c-Jun N-terminal kinase. 5. The results provide the first evidence that fucoidan has a potent inhibitory effect against LPS-induced NO production by microglia. The results also suggest that this inhibitory action of fucoidan involves suppression of p38 and ERK phosphorylation.
Insights
Fucoidan, a seaweed extract, effectively inhibits lipopolysaccharide (LPS)-induced nitric oxide (NO) production in microglia. This anti-inflammatory action involves suppressing key signaling pathways like p38 and ERK, offering potential therapeutic benefits for neuroinflammation.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Microglial activation contributes to neuroinflammation and neurodegeneration via pro-inflammatory cytokines.
- Microglia-derived nitric oxide (NO) is crucial in lipopolysaccharide (LPS)-induced dopaminergic neuron loss.
- Fucoidan, a sulfated polysaccharide from brown seaweeds, exhibits anti-inflammatory properties.
Purpose of the Study:
- To investigate fucoidan's effects on LPS-induced microglial activation.
- To elucidate the inhibitory mechanisms of fucoidan in microglia.
- To assess fucoidan's impact on nitric oxide production and inflammatory markers.
Main Methods:
- Primary microglial cells were pre-treated with varying concentrations of fucoidan before LPS stimulation.
- Assessed cell morphology, nitric oxide (NO) production, and inducible nitric oxide synthase (iNOS) expression (mRNA and protein).
- Evaluated mitogen-activated protein kinase (MAPK) pathway activation, including p38, ERK, and JNK.
Main Results:
- Fucoidan inhibited LPS-induced microglial cell shape changes.
- High-dose fucoidan significantly reduced NO production and iNOS expression.
- Fucoidan suppressed phosphorylation of p38 and ERK, but not JNK.
Conclusions:
- Fucoidan demonstrates potent inhibition of LPS-induced NO production in microglia.
- The anti-inflammatory effects of fucoidan are mediated through the suppression of p38 and ERK signaling pathways.
- Fucoidan shows promise as a therapeutic agent for neuroinflammatory conditions.
