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.
Keywords: Apostichopus japonicus; Autophagy; Fucoidan; Inflammation; RAW264.7 cells.
© 2025. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.