β-Linked polysaccharides including β-glucans are well known to be important functional ingredients, and are known to possess immunomodulatory and anti-tumor activities. This study aimed to investigate the anti-inflammatory properties and participating receptor of water soluble and insoluble bioactive polysaccharides from Grifola frondosa (GFP, non-digestible water soluble polysaccharides), Laminaria digitata (laminarin, a water soluble β-glucan) and Saccharomyces cerevisiae (zymosan, a water insoluble β-glucan) in lipopolysaccharide (LPS)-stimulated parental and Dectin-1 highly expressing RAW264.7 macrophages. Results showed that GFP and laminarin significantly inhibited nitric oxide and prostaglandin E2 production, but only the GFP with high molecular weight exhibited strong inhibition on pro-inflammatory cytokine (TNF-α and IL-6) secretion in a concentration-dependent manner. The activation of NF-κB was also significantly down-regulated by GFP treatment as compared with cells treated with LPS alone. Although GFP and laminarin were able to bind to β-glucan receptor Dectin-1, there was no relationship between the inhibitory potency and the content of β-glucans in GFP, and these inhibitory effects were not affected by the expression level of Dectin-1 in macrophage cells. In contrast, zymosan significantly intensified LPS-induced inflammatory responses through Dectin-1. In conclusion, these results suggest that the inhibitory effects of water soluble polysaccharides on LPS-induced pro-inflammatory mediator production in murine macrophages may not involve β-glucan receptor Dectin-1.

众所周知，包括 β-葡聚糖在内的 β-多糖是重要的功能成分，并且具有免疫调节和抗肿瘤活性。本研究旨在研究来自灰树花（GFP，不可消化的水溶性多糖）、海带（海带多糖，一种水溶性 β-葡聚糖）和酿酒酵母的水溶性和不溶性生物活性多糖的抗炎特性和参与受体（酵母聚糖，一种水不溶性 β-葡聚糖）在脂多糖 (LPS) 刺激的亲本和高表达 RAW264.7 巨噬细胞中的 Dectin-1。结果表明，GFP和海带多糖显着抑制一氧化氮和前列腺素E2的产生，但只有高分子量的GFP以浓度依赖性方式对促炎细胞因子（TNF-α和IL-6）分泌表现出强抑制作用。与单独用 LPS 处理的细胞相比，GFP 处理也显着下调了 NF-κB 的激活。尽管GFP和海带多糖能够与β-葡聚糖受体Dectin-1结合，但抑制效力与GFP中β-葡聚糖含量无关，且这些抑制作用不受Dectin-1表达水平的影响在巨噬细胞中。相比之下，酵母聚糖通过 Dectin-1 显着增强 LPS 诱导的炎症反应。总之，这些结果表明水溶性多糖对 LPS 诱导的鼠巨噬细胞促炎介质产生的抑制作用可能不涉及 β-葡聚糖受体 Dectin-1。