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.

中文翻译：

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硫酸化多糖对巨噬细胞中晚期糖基化终产物摄取和清除剂受体A类水平影响的比较研究。

高级糖基化终产物，尤其是衍生自甘油醛（高级糖基化终产物2）和乙醇醛（高级糖基化终产物3）的有毒高级糖基化终产物，是与糖尿病并发症相关的生物活性化合物。我们以前证明毒性高级糖基化终产物通过清除剂受体1 A类（CD204）被内化为巨噬细胞样RAW264.7细胞。岩藻依聚糖（一种硫酸化多糖和清道夫受体的拮抗配体）可抑制有毒的晚期糖基化终产物摄取，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。在这个研究中，我们比较了六种类型的硫酸化和非硫酸化多糖对RAW264.7细胞中毒性高级糖基化终产物摄取的影响。褐藻糖胶，角叉菜胶和硫酸葡聚糖减弱了毒性高级糖化终产物的摄取。岩藻聚糖和角叉菜胶抑制糖基化终产物2诱导的SR-A的上调，而糖基化终产物3诱导的清道夫受体1 A类的上调仅被岩藻依聚糖抑制。硫酸右旋糖酐不会影响毒性高级糖基化终产物处理细胞中的清道夫受体-1 A类水平。硫酸软骨素，肝素和透明质酸未能减弱有毒晚期糖基化终产物的摄取。肝素和透明质酸对清除剂受体1 A类水平没有影响，