Dataset Information

Fucoidan protects against lipopolysaccharide-induced rat neuronal damage and inhibits the production of proinflammatory mediators in primary microglia.

ABSTRACT:

Background

Fucoidan, a sulfated polysaccharide extracted from brown algae, possesses potent antiinflammatory effects.

Aims

To examine the effect of fucoidan treatment on inflammation-mediated dopaminergic neuronal damage and its potential mechanisms.

Methods

Microglial activation and injury of dopaminergic neurons were induced by intranigral injection of lipopolysaccharide (LPS), and the effects of fucoidan treatment on animal behavior, microglial activation and survival ratio of dopaminergic neurons were investigated. We further observed the efficacy of fucoidan on tumor necrosis factor-alpha (TNF-?) and the production of reactive oxygen species (ROS) in LPS-activated primary microglia.

Results

Fucoidan significantly improved the behavioral manifestation, prevented the loss of dopaminergic neurons and inhibited the deleterious activation of microglia in the substantia nigra pars compacta of LPS-treated rats. Further in vitro experiments indicated that the excessive production of TNF-? and ROS in LPS-induced primary microglia were significantly inhibited by fucoidan administration.

Conclusion

This is the first study to demonstrate that fucoidan possesses neuroprotective effects on injured dopaminergic neurons in a LPS-induced animal model of Parkinson's disease. The mechanisms underlying these effects may include its potent down-regulation of intracellular ROS and subsequent proinflammatory cytokine release in LPS-activated microglia.

SUBMITTER: Cui YQ

PROVIDER: S-EPMC6493380 | biostudies-literature | 2012 Oct

REPOSITORIES: biostudies-literature

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Publications

Fucoidan protects against lipopolysaccharide-induced rat neuronal damage and inhibits the production of proinflammatory mediators in primary microglia.

Cui Yan-Qiu YQ Jia Yan-Jun YJ Zhang Ting T Zhang Quan-Bin QB Wang Xiao-Min XM

CNS neuroscience & therapeutics 20121001 10

<h4>Background</h4>Fucoidan, a sulfated polysaccharide extracted from brown algae, possesses potent antiinflammatory effects.<h4>Aims</h4>To examine the effect of fucoidan treatment on inflammation-mediated dopaminergic neuronal damage and its potential mechanisms.<h4>Methods</h4>Microglial activation and injury of dopaminergic neurons were induced by intranigral injection of lipopolysaccharide (LPS), and the effects of fucoidan treatment on animal behavior, microglial activation and survival ra ...[more]

PMID: 23006515

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Project description:Inflammation has long been implicated as a contributor to pathogenesis in many CNS illnesses, including Lyme neuroborreliosis. Borrelia burgdorferi is the spirochete that causes Lyme disease and it is known to potently induce the production of inflammatory mediators in a variety of cells. In experiments where B. burgdorferi was co-cultured in vitro with primary microglia, we observed robust expression and release of IL-6 and IL-8, CCL2 (MCP-1), CCL3 (MIP-1alpha), CCL4 (MIP-1beta) and CCL5 (RANTES), but we detected no induction of microglial apoptosis. In contrast, SH-SY5Y (SY) neuroblastoma cells co-cultured with B. burgdorferi expressed negligible amounts of inflammatory mediators and also remained resistant to apoptosis. When SY cells were co-cultured with microglia and B. burgdorferi, significant neuronal apoptosis consistently occurred. Confocal microscopy imaging of these cell cultures stained for apoptosis and with cell type-specific markers confirmed that it was predominantly the SY cells that were dying. Microarray analysis demonstrated an intense microglia-mediated inflammatory response to B. burgdorferi including up-regulation in gene transcripts for TLR-2 and NFkappabeta. Surprisingly, a pathway that exhibited profound changes in regard to inflammatory signaling was triggering receptor expressed on myeloid cells-1 (TREM1). Significant transcript alterations in essential p53 pathway genes also occurred in SY cells cultured in the presence of microglia and B. burgdorferi, which indicated a shift from cell survival to preparation for apoptosis when compared to SY cells cultured in the presence of B. burgdorferi alone. Taken together, these findings indicate that B. burgdorferi is not directly toxic to SY cells; rather, these cells become distressed and die in the inflammatory surroundings generated by microglia through a bystander effect. If, as we hypothesized, neuronal apoptosis is the key pathogenic event in Lyme neuroborreliosis, then targeting microglial responses may be a significant therapeutic approach for the treatment of this form of Lyme disease.

Dataset Information

Fucoidan protects against lipopolysaccharide-induced rat neuronal damage and inhibits the production of proinflammatory mediators in primary microglia.

Background

Aims

Methods

Results

Conclusion

Publications

Fucoidan protects against lipopolysaccharide-induced rat neuronal damage and inhibits the production of proinflammatory mediators in primary microglia.

Similar Datasets

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