Sun Xialin, Zhang Tingwen, Zhao Yan, Yang Han, Li Yawei, Sun Xin, Bian Xingbo
School of Pharmaceutical Sciences, Jilin Medical University, China.
College of Chinese Medicinal Materials, Jilin Agricultural University, China.
Int J Biol Macromol. 2025 Sep;321(Pt 3):146421. doi: 10.1016/j.ijbiomac.2025.146421. Epub 2025 Jul 31.
Ulcerative colitis (UC) involves intestinal barrier dysfunction, immune dysregulation, and microbiota imbalance. Bletilla striata polysaccharide (BSP) shows anti-inflammatory potential, but its UC mechanisms remain unclear.
To purify Bletilla striata polysaccharide (BSP-1), characterize its structure, and elucidate its multi-target UC therapeutic mechanisms.
This study purified a novel structure of neutral glucomannan with a small amount of acetylation (BSP-1). Together with tight junction protein analysis, oxidative stress markers, 16S rRNA sequencing, cytokine quantification, and molecular ecological network examination, the team used a UC mouse model created using dextran sodium sulfate (DSS).
BSP-1 alleviated colitis by inhibiting TLR4/MyD88/NF-κB signaling (elevating IL-10; lowering IL-6, TNF-α, and IL-1β) and restoring integrity of the intestinal barrier via upregulating Occludin, ZO-1, MUC2, and Claudin-1. It reduced oxidative stress (lower MDA; higher SOD) and modulated gut microbiota (enriched Lactobacillus, suppressed Escherichia-Shigella). Molecular ecological network analysis showed that BSP-1 restored microbial community stability by enhancing bacterial competition.
BSP-1 exerts integrated anti-inflammatory, barrier-repairing, and microbiota-regulating effects, highlighting its potential as a multi-target UC therapy and intestinal microecological regulator.
溃疡性结肠炎(UC)涉及肠道屏障功能障碍、免疫失调和微生物群失衡。白及多糖(BSP)具有抗炎潜力,但其治疗UC的机制尚不清楚。
纯化白及多糖(BSP-1),表征其结构,并阐明其多靶点治疗UC的机制。
本研究纯化了一种新结构的、带有少量乙酰化的中性葡甘露聚糖(BSP-1)。研究团队结合紧密连接蛋白分析、氧化应激标志物、16S rRNA测序、细胞因子定量和分子生态网络检测,使用葡聚糖硫酸钠(DSS)建立UC小鼠模型。
BSP-1通过抑制TLR4/MyD88/NF-κB信号传导(提高IL-10;降低IL-6、TNF-α和IL-1β)以及上调闭合蛋白、紧密连接蛋白1、黏蛋白2和Claudin-1来恢复肠道屏障的完整性,从而减轻结肠炎。它降低了氧化应激(降低丙二醛;提高超氧化物歧化酶)并调节肠道微生物群(富集乳酸杆菌,抑制埃希氏菌属-志贺氏菌属)。分子生态网络分析表明,BSP-1通过增强细菌竞争来恢复微生物群落稳定性。
BSP-1发挥综合抗炎、屏障修复和微生物群调节作用,突出了其作为多靶点UC治疗药物和肠道微生态调节剂的潜力。