本研究旨在探索从华北马鞍草中提取的一种四糖——佛手糖的抗炎作用。使用脂多糖（LPS）刺激的RAW264.7巨噬细胞模型和戊二醛钠（DSS）诱导的溃疡性结肠炎（UC）BALB/C小鼠模型评估了佛手糖的体内外抗炎作用。采用酶联免疫吸附法（ELISA）检测亚硝酸盐（NO）和细胞因子（白细胞介素-1β，白细胞介素-6，肿瘤坏死因子-α）的水平，并使用苏木精伊红染色观察小鼠肠道形态的变化。此外，还探究了反转录-聚合酶链式反应（RT-qPCR）和西方印迹的可能机制。结果表明，佛手糖和其他四种低聚糖（半乳糖低聚糖，木糖低聚糖，菊粉和耐性糊精）能以剂量依赖的方式抑制LPS刺激的RAW264.7巨噬细胞的NO分泌和促炎性细胞因子的产生，其中佛手糖在体外效果最好。在小鼠体内，不同剂量的佛手糖显著缓解了DSS诱导的溃疡性结肠炎症状，并且佛手糖也显著抑制了体内炎性细胞因子和髓过氧化物酶（MPO）的产生。此外，我们的研究发现，佛手糖能够抑制TLR4的表达，并在体内外抑制NF-κB p65的磷酸化。总之，结果表明，佛手糖通过抑制TLR4/NF-κB信号通路发挥抗炎作用。本文受版权保护，所有权利均为本文作者所有。

This study aimed to explore the anti-inflammatory effect of stachyose, a tetrasaccharide extracted from Stachys sieboldii Miq. A lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages model and a dextran sodium sulfate (DSS)-induced ulcerative colitis (UC) BALB/C mice model was used to assess the anti-inflammatory effect of stachyose both in vitro and in vivo. The levels of Nitric oxide (NO) and cytokines (Interleukin-1β, Interleukin-6, Tumor necrosis factor-α) were detected using enzyme-linked immunosorbent assay (ELISA) methods; besides, hematoxylin-eosin (HE) staining was used to observe changes in intestinal morphology of mice. In addition, the possible mechanisms were explored by reverse transcription-polymerase chain reaction (RT-qPCR) and western blot. Results showed that stachyose and four other oligosaccharides (galacto-oligosaccharides, xylo-oligosaccharides, inulin and resistant dextrin) inhibited NO secretion and the production of pro-inflammatory cytokines in LPS-stimulated RAW264.7 macrophages in a dose-dependent manner, while stachyose was most effective in vitro. In mice, different doses of stachyose significantly alleviated the symptoms of DSS-induced ulcerative colitis and stachyose also significantly inhibited the production of inflammatory cytokines and myeloperoxidase (MPO) in vivo. In addition, our findings illustrated that stachyose inhibited expression of TLR4 and suppressed the phosphorylation of NF-κB p65 both in vitro and in vivo. Taken together, results demonstrated that stachyose exerted anti-inflammatory effect through inhibition of the TLR4/NF-κB signaling pathway. This article is protected by copyright. All rights reserved.This article is protected by copyright. All rights reserved.