Hou Tingting, Liu Xiaolin, Zhang Shuai, Tang Kui, Liu Shilin, Liu Jialiang, Fan Xiaoteng, Wang Zaizhao
College of Animal Science and Technology, Northwest A&F University, 22 Xinong Road, Yangling, Xianyang, 712100, Shaanxi, China.
CAS Key Laboratory of Marine Ecology and Environmental Sciences, Institute of Oceanology, Chinese Academy of Sciences, Qingdao, 266071, China.
Mar Biotechnol (NY). 2025 Jan 20;27(1):32. doi: 10.1007/s10126-025-10410-7.
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.
来自刺参的岩藻多糖（Aj-FUC）已显示出抗炎活性，但其作用机制尚未阐明。本研究调查了绿色和紫色刺参中的岩藻多糖（G-FUC和P-FUC）在脂多糖（LPS）处理的RAW264.7细胞中的抗炎潜力及机制。结果表明，在24小时刺激后，25 - 400µg/mL的Aj-FUC对细胞无毒性，并促进细胞吞噬活性。ELISA结果表明，Aj-FUC降低了一氧化氮（NO）、肿瘤坏死因子α（TNF-α）、白细胞介素-1β（IL-1β）和IL-6水平，并提高了IL-10水平。Aj-FUC抑制了LPS处理的RAW264.7细胞中炎症相关基因（tnf-α、il-1β、il-6、nlrp3、inos、cox-2、tlr4、trif和nf-κb）的转录，其中G-FUC具有更强的抗炎作用。此外，Aj-FUC上调了自噬基因（beclin1、lc3II和lamp2）的mRNA表达。Beclin-1和LC3II的免疫印迹和免疫荧光分析支持Aj-FUC增强了自噬活性。在用3-甲基腺嘌呤抑制自噬后，在LPS诱导的经Aj-FUC处理的细胞中，tnf-α、il-6、il-1β和nlrp3的mRNA表达显著上调，表明Aj-FUC通过自噬介导抑制炎症。总之，本研究表明Aj-FUC通过提高LPS诱导的巨噬细胞中的自噬活性发挥抗炎作用。
