基于根茎Stemonaceae科植物Stemona tuberosa Lour的低分子量多糖在抗菌休克诱导的急性肺损伤中的抗炎活性及其机制
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
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影响因子:8.5
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
DOI:
10.1016/j.ijbiomac.2024.136617
摘要
Stemona tuberosa Lour的根茎一直用于治疗结核病、疥疮和湿疹。多糖是其主要的生物活性成分之一。通过优化三相分配法获得了一种分子量较低（1819 Da）的多糖（SPS2-A），并利用离子色谱柱纯化，研究其作用机制。结构分析显示，SPS2-A含有阿拉伯糖、半乳糖（Gal）、葡萄糖（Glc）、木糖和甘露糖。SPS2-A的主链结构包括糖残基→4)-α-D-Glcp-(1→、→4)-α-D-Galp-(1→及→4,6)-β-D-Galp-(1→，侧链主要由α-D-Glcp-(1→连接到残基→4,6)-β-D-Galp-(1→的O-6位置。在体外实验中，SPS2-A能下调脂多糖诱导的RAW264.7巨噬细胞中白细胞介素-6的表达。在体内实验中，SPS2-A显著下调肺泡灌洗液和肺组织中髓过氧化物酶、白细胞介素-6、白细胞介素-1β和肿瘤坏死因子-α的表达。免疫印迹分析表明，SPS2-A通过激活核因子κB（NF-κB）途径，减轻了败血症引起的急性肺损伤的小鼠肺部炎症。这些结果提示，SPS2-A或可作为治疗败血症引发的急性肺损伤的潜在抗炎候选分子。
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.