ArticleMarine biotechnology (New York, N.Y.)2025
Anti-inflammatory Effects of the Fucoidan from Sea Cucumber Apostichopus japonicus.
Article in Marine biotechnology (New York, N.Y.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Ferulic Acid Alleviates Intestinal Inflammatory Damage in Mice, Associated with Ameliorating Intestinal Barrier Damage and Gut Microbiota.Animals : an open access journal from MDPI · 2025Article
- Research progress on natural products in regulating the gut microbiota in Parkinson's disease.Frontiers in pharmacology · 2025Review
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8 authors.
Funding
Abstract
Fucoidan from Apostichopus japonicus (Aj-FUC) has shown anti-inflammatory activity, whereas its mechanism was not explicated. This study investigated the anti-inflammatory potential and mechanism of the fucoidan from green and purple A. japonicus (G-FUC and P-FUC) in lipopolysaccharide (LPS)-treated RAW264.7 cells. Results showed that Aj-FUCs at 25-400 µg/mL had no toxicity to cells after 24 h stimulation and promoted cell phagocytic activity. ELISA results indicated that Aj-FUC reduced the nitric oxide (NO), tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), and IL-6 levels and increased IL-10 level. The Aj-FUC suppressed transcription of inflammatory-related genes (tnf-α, il-1β, il-6, nlrp3, inos, cox-2, tlr4, trif, and nf-κb) in LPS-treated RAW264.7 cells, among which G-FUC had stronger anti-inflammatory effects. Moreover, Aj-FUC upregulated the mRNA expression of autophagic genes (beclin1, lc3II, and lamp2). The immunoblotting and immunofluorescence analyses of Beclin-1 and LC3II supported that Aj-FUC enhanced autophagy activity. After autophagy inhibited by 3-methyladenine, the mRNA expressions of tnf-α, il-6, il-1β, and nlrp3 were significantly upregulated in LPS-induced cells treated with Aj-FUC, suggesting the suppressed inflammation by Aj-FUC mediated via autophagy. Summarily, the present study demonstrated that Aj-FUC showed anti-inflammatory effects by elevating autophagy activity in LPS-induced macrophages.
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