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<p>Fucoidan from <i>Apostichopus japonicus</i> (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 <i>A. japonicus</i> (G-FUC and P-FUC) in lipopolysaccharide (LPS)-treated RAW264.7 cells. Results showed that Aj<i>-</i>FUCs at 25–400&#xa0;µg/mL had no toxicity to cells after 24&#xa0;h stimulation and promoted cell phagocytic activity. ELISA results indicated that Aj<i>-</i>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 (<i>tnf-α, il-1β</i>, <i>il-6</i>, <i>nlrp3</i>, <i>inos</i>, <i>cox-2</i>, <i>tlr4</i>, <i>trif</i>, and <i>nf-κb</i>) in LPS-treated RAW264.7 cells, among which G-FUC had stronger anti-inflammatory effects. Moreover, Aj<i>-</i>FUC upregulated the mRNA expression of autophagic genes (<i>beclin1</i>, <i>lc3II</i>, and <i>lamp2</i>). The immunoblotting and immunofluorescence analyses of Beclin-1 and LC3II supported that Aj<i>-</i>FUC enhanced autophagy activity. After autophagy inhibited by 3-methyladenine, the mRNA expressions of <i>tnf-α</i>, <i>il-6</i>, <i>il-1β</i>, and <i>nlrp3</i> 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<i>-</i>FUC showed anti-inflammatory effects by elevating autophagy activity in LPS-induced macrophages.</p> Graphical Abstract <p></p>

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Anti-inflammatory Effects of the Fucoidan from Sea Cucumber Apostichopus japonicus

  • 期刊论文

  • 发表日期：

    2025年1月20日

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  • Tingting Hou,
  • Xiaolin Liu,
  • Shuai Zhang,
  • Kui Tang,
  • Shilin Liu,
  • Jialiang Liu,
  • Xiaoteng Fan,
  • Zaizhao Wang

摘要

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.

Graphical Abstract