Structural characterization and anti-osteoporosis effects of polysaccharide purified from Eucommia ulmoides Oliver cortex based on its modulation on bone metabolism
Structural characterization and anti-osteoporosis effects of polysaccharide purified from Eucommia ulmoides Oliver cortex based on its modulation on bone metabolism
复制标题
杜仲多糖的结构表征及基于其对骨代谢调节的抗骨质疏松作用
DOI：
10.1016/j.carbpol.2023.120601
复制
发表时间：
2023
影响因子：
11.2
通讯作者：
Min Hu
中科院分区：
文献类型：
--
作者：
Jiyu Song;Yongfeng Zhang;Yanfeng Zhu;Xinghui Jin;Lanzhou Li;Chunyue Wang;Ying Zhou;Yutong Li;Di Wang;Min Hu
EuOCP 3是从杜仲皮中分离得到的一种酸性多糖，分子量为38.1kDa。EuOCP_3的主链主要由→ 4）-α-GalpA-（1 → 4）-α-GalpA-（1 →，→ 4）-α-GalpA-（1 → 5）-α-Araf-（1 →，→ 4）-α-GalpA-（1 → 2）-α-Rhap-（1 → 2）-α-GalpA-（1 → 4）-α-GalpA-（1 → 4）-α-GalpA-（1 → 5）-α-Araf-（1 →，→ 4）-α-GalpA-（1 → 2）-α-Rhap-（1 → 4）-α-GalpA-（1 → 5）-α-Araf-（1 →，→ 4）-α-GalpA-（1 → 2）-α-Rhap-（1 → 4）-α-GalpA-（1 → 5）-α-Araf-（1 → 4）-α-GalpA-（1 → 2）-Rhap-（1 → 2）-α-Rhap-（1 →（1 →，和→ 4）-α-GalpA-（1 → 5）-α-Araf-（1 → 2）-α-Rhap-（1 →）重复嵌段通过→ 2，3，5）-α-Araf-（1 →）连接。在→ 2，3，5）-α-Araf-（1 →）侧链的C-2和C-5位取代，含有T-β-Araf →和T-β-Araf → 4）-α-GalpA-（1 →）残基。在地塞米松（Dex）诱导的骨质疏松症（OP）小鼠中，EuOCP3治疗恢复了皮质骨厚度，增加了矿化骨面积，增加了成骨细胞的数量，并减少了皮质骨表面破骨细胞的数量。结合肠道菌群、血清代谢产物谱和生物学检测结果的分析，我们证明EuOCP3调节肠道菌群中特定物种的丰度，如g_Dorea和g_Prevotella，并改善氧化应激。反过来，通过细胞外信号调节激酶（ERK）/c-Jun N-末端激酶（JNK）/核因子红细胞-2相关因子2（Nrf2）信号通路，表明成骨功能增强和骨代谢恢复。目前的研究结果有助于了解EuOCP3在抗OP治疗中的潜力。
EuOCP3, with a molecular weight of 38.1 kDa, is an acidic polysaccharide purified fromEucommia ulmoidesOliver cortex. Herein, we determined that the main backbone of EuOCP3 was predominantly composed of →4)-α-GalpA-(1 → 4)-α-GalpA-(1→, →4)-α-GalpA-(1 → 5)-α-Araf-(1→, →4)-α-GalpA-(1 → 2)-α-Rhap-(1→, and →4)-α-GalpA-(1 → 5)-α-Araf-(1 → 2)-α-Rhap-(1 → repeating blocks, which were connected by →2,3,5)-α-Araf-(1→. The side chains, substituted at C-2 and C-5 of →2,3,5)-α-Araf-(1→, contained T-β-Araf→ and T-β-Araf→ 4)-α-GalpA-(1 → residues. In dexamethasone (Dex)-induced osteoporosis (OP) mice, EuOCP3 treatment restored cortical bone thickness, increased mineralized bone area, enhanced the number of osteoblasts, and decreased the number of osteoclasts on the surface of cortical bone. Combining analysis of gut microflora, serum metabolite profiles, and biological detection results, we demonstrated that EuOCP3 regulated the abundance of specific species within the gut microflora, such asg_Doreaandg_Prevotella, and ameliorated oxidative stress. In turn, enhancement of osteogenic function and restoration of bone metabolism via the extracellular signal-regulated kinase (ERK)/c-Jun N-terminal kinase (JNK)/nuclear factor erythroid-2 related factor 2 (Nrf2) signaling pathway was indicated. The current findings contribute to understanding the potential of EuOCP3 in anti-OP treatment.