Anti-Neuroinflammatory Effects of a Representative Low-Molecular-Weight Component Isolated from Codium fragile Through Inhibition of the NF-κB Pathway in Microglia and Macrophage Cells

TL;DR

This study shows that a compound from Codium fragile can reduce neuroinflammation by blocking a key inflammatory pathway in brain cells.

Contribution

The novel contribution is identifying uracil in Codium fragile as an anti-neuroinflammatory agent through NF-κB inhibition.

Findings

AECF and uracil reduced pro-inflammatory cytokine production in LPS-stimulated cells.

The NF-κB pathway was suppressed by AECF and uracil in microglia and macrophage cells.

Uracil was identified as a major low-molecular-weight component in Codium fragile.

Abstract

The worldwide incidence of neurodegenerative diseases (ND), such as dementia, has increased, and neuroinflammation is considered a crucial factor in the development of ND. Codium fragile is considered ocean waste in many countries; however, some countries, including Korea, consume it as a food resource. In this study, a major low-molecular-weight component and chemical marker, uracil, was isolated from the aqueous extracts of C. fragile (AECF); additionally, its content was measured through HPLC quantitative analysis. AECF and uracil were examined for their anti-inflammatory activities against lipopolysaccharide (LPS)-stimulated BV2 microglia and RAW264.7 macrophage cell lines under inflammation conditions. The results showed that AECF and uracil inhibited the production of pro-inflammatory cytokines by suppressing the NF-κB pathway.

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