抗炎活性和潜在机制，可抵抗败血症诱导的急性肺损伤，从stemona tuberosa lour的根部产生低分子量多糖
Anti-inflammatory activity and underlying mechanism against sepsis-induced acute lung injury of a low-molecular-weight polysaccharide from the root of Stemona tuberosa Lour
影响因子:8.50000
分区:生物学2区 Top / 生化与分子生物学2区 应用化学2区 高分子科学2区
发表日期:2024 Dec
作者:
Xiang Qiu, Yan Geng, Xiaoyue Cai, Yanghui Ou, Mengjie Li, Yali Zhang, Dengqin He, Xudong Qian, Yanting Wu, Hongwei Ma, Jing-Kun Yan, Hongliang Yao, Wen-Hua Chen
摘要
stemona tuberosa lour的根源已用于治疗结核病，s虫和湿疹。多糖是其主要的生物活性成分之一。通过优化三相分配，使用离子色谱柱进行纯化，研究了低分子量（1819 DA）多糖（SPS2-A），并研究了其效果和机制。结构分析表明，SPS2-A包含阿拉伯糖，半乳糖（GAL），葡萄糖（GLC），木糖和甘露糖。 SPS2-A主链结构包含糖残基→4）-α-D-GLCP-（1→，→4）-α-d-d-galp-（1→→4,6）-β-d-d-galp-（1→1→，而侧链主要组成α-d-d-d-d-glcp-（1→→1→O-6的残基位置， →4,6)-β-D-Galp-(1→. In vitro, SPS2-A downregulated the expression of interleukin-6 in lipopolysaccharide-induced RAW264.7 macrophages. In vivo, SPS2-A significantly downregulated the expression of myeloperoxidase, interleukin-6, interleukin-1β, and tumor necrosis factor-α in bronchoalveolar灌洗液和肺部印迹分析表明，SPS2-A通过激活核因子κB途径而降低了败血症诱导的急性肺损伤的肺部炎症。
Abstract
The root of Stemona tuberosa Lour has been used to treat tuberculosis, scabies, and eczema. Polysaccharides are among its main bioactive ingredients. A low-molecular-weight (1819 Da) polysaccharide (SPS2-A) was obtained from the root of S. tuberosa Lour by optimizing three-phase partitioning, purified using an ion chromatography column, and its effects and mechanisms were investigated. Structural analysis revealed that SPS2-A contained arabinose, galactose (Gal), glucose (Glc), xylose, and mannose. The SPS2-A backbone structure comprised sugar residues →4)-α-D-Glcp-(1→, →4)-α-D-Galp-(1→, and →4,6)-β-D-Galp-(1→, while the side chain primarily comprised α-D-Glcp-(1 → connected to the O-6 position of the residue →4,6)-β-D-Galp-(1→. In vitro, SPS2-A downregulated the expression of interleukin-6 in lipopolysaccharide-induced RAW264.7 macrophages. In vivo, SPS2-A significantly downregulated the expression of myeloperoxidase, interleukin-6, interleukin-1β, and tumor necrosis factor-α in bronchoalveolar lavage fluid and lung tissue. Western blotting analysis indicated that SPS2-A reduced lung inflammation in mice with sepsis-induced acute lung injury by activating the nuclear factor κB pathway. These results suggest that SPS2-A is a potential anti-inflammatory candidate for the treatment of sepsis-induced acute lung injury.