A comparative study of sulphated polysaccharide effects on advanced glycation end-product uptake and scavenger receptor class A level in macrophages.
A comparative study of sulphated polysaccharide effects on advanced glycation end-product uptake and scavenger receptor class A level in macrophages.
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DOI：
10.1177/1479164119896975
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发表时间：
2020-01
影响因子：
2.4
通讯作者：
Takahashi H
中科院分区：
文献类型：
--
作者：
Nishinaka T;Mori S;Yamazaki Y;Niwa A;Wake H;Yoshino T;Nishibori M;Takahashi H
晚期糖基化终产物，特别是来自甘油醛（晚期糖基化终产物-2）和乙醇醛（晚期糖基化终产物-3）的毒性晚期糖基化终产物，是与糖尿病并发症相关的生物反应性化合物。我们以前证明，有毒的晚期糖基化终产物通过清道夫受体-1 A类（CD 204）内化到巨噬细胞样RAW264.7细胞中。岩藻聚糖（一种硫酸化多糖和清道夫受体的拮抗性配体）可以抑制毒性晚期糖基化终产物的摄入，这表明硫酸化多糖是治疗晚期糖基化终产物相关疾病的新兴候选药物。在这项研究中，我们比较了六种类型的硫酸化和非硫酸化多糖的毒性晚期糖基化终产物摄取在RAW 264.7细胞的影响。褐藻糖胶、角叉菜胶和硫酸葡聚糖减弱了毒性晚期糖基化终产物的摄取。褐藻糖胶和卡拉胶抑制晚期糖基化终产物-2诱导的SR-A上调，而晚期糖基化终产物-3诱导的清道夫受体-1 A类上调仅被褐藻糖胶抑制。硫酸葡聚糖不影响毒性晚期糖基化终产物处理细胞中清道夫受体-1 A类水平。硫酸软骨素、肝素和透明质酸未能减弱毒性晚期糖基化终产物摄取。肝素和透明质酸对清道夫受体-1 A类水平没有影响，而硫酸软骨素抑制晚期糖基化终产物-3诱导的清道夫受体-1 A类上调。两者合计，岩藻依聚糖和角叉菜胶，但不是其他硫酸化多糖检查，有抑制活性的毒性晚期糖基化终产物的摄取和毒性晚期糖基化终产物诱导的清道夫受体-1 A类的上调，可能是因为硫酸化多糖之间的结构差异。
Advanced glycation end-products, especially toxic advanced glycation end-products derived from glyceraldehyde (advanced glycation end-product-2) and glycolaldehyde (advanced glycation end-product-3), are biologically reactive compounds associated with diabetic complications. We previously demonstrated that toxic advanced glycation end-products were internalised into macrophage-like RAW264.7 cells through scavenger receptor-1 class A (CD204). Toxic advanced glycation end-product uptake was inhibited by fucoidan, a sulphated polysaccharide and antagonistic ligand for scavenger receptors, suggesting that sulphated polysaccharides are emerging candidates for treatment of advanced glycation end-product–related diseases. In this study, we compared the effects of six types of sulphated and non-sulphated polysaccharides on toxic advanced glycation end-product uptake in RAW264.7 cells. Fucoidan, carrageenan and dextran sulphate attenuated toxic advanced glycation end-product uptake. Fucoidan and carrageenan inhibited advanced glycation end-product-2–induced upregulation of SR-A, while advanced glycation end-product-3–induced upregulation of scavenger receptor-1 class A was only suppressed by fucoidan. Dextran sulphate did not affect scavenger receptor-1 class A levels in toxic advanced glycation end-product–treated cells. Chondroitin sulphate, heparin and hyaluronic acid failed to attenuate toxic advanced glycation end-product uptake. Heparin and hyaluronic acid had no effect on scavenger receptor-1 class A levels, while chondroitin sulphate inhibited advanced glycation end-product-3–induced upregulation of scavenger receptor-1 class A. Taken together, fucoidan and carrageenan, but not the other sulphated polysaccharides examined, had inhibitory activities on toxic advanced glycation end-product uptake and toxic advanced glycation end-product–induced upregulation of scavenger receptor-1 class A, possibly because of structural differences among sulphated polysaccharides.
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影响因子：
10.9
作者：
Manigrasso, Michaele B.;Juranek, Judyta;Ramasamy, Ravichandran;Schmidt, Ann Marie
通讯作者：
Schmidt, Ann Marie
影响因子：
--
作者：
Platt, N;Gordon, S
通讯作者：
Gordon, S
影响因子：
11.2
作者：
Lee, Seung-Hong;Ko, Chang-Ik;Jeon, You-Jin
通讯作者：
Jeon, You-Jin
影响因子：
10.7
作者：
Langendorff, V;Cuvelier, G;De kruif, CG
通讯作者：
De kruif, CG
影响因子：
6.7
作者：
Campa, VM;Iglesias, JM;Lazo, PS
通讯作者：
Lazo, PS