Polysulfated glycosaminoglycan accelerates net synthesis of collagen and glycosaminoglycans by arthritic equine cartilage tissues and chondrocytes.
Polysulfated glycosaminoglycan accelerates net synthesis of collagen and glycosaminoglycans by arthritic equine cartilage tissues and chondrocytes.
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多硫酸化糖胺聚糖可加速关节炎马软骨组织和软骨细胞的胶原蛋白和糖胺聚糖的净合成。
DOI：
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发表时间：
1990
影响因子：
1
通讯作者：
Michael J. Glade
中科院分区：
文献类型：
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作者：
Michael J. Glade
在器官培养中，低分子量多硫酸化糖胺聚糖（PSGAG）刺激正常和关节炎马胚软骨组织的净胶原和糖胺聚糖合成。关节炎组织对PSGAG刺激更敏感。软骨特异性II型胶原蛋白和硫酸软骨素丰富的糖胺聚糖的合成率从正常和关节炎的马软骨组织获得的融合软骨细胞培养物增加了25和50毫克的PSGAG/毫升。来自关节炎软骨的细胞对PSGAG的存在也更敏感。此外，关节内注射250 mg PSGAG后，PSGAG浓度（25和50 mg/ml）接近滑液中的浓度，可抑制细胞培养物中胶原和糖胺聚糖降解的速率。这些发现表明，PSGAG可能通过促进替代透明基质材料的产生，同时延迟其随后的降解，在轻度软骨退变的愈合中发挥作用。相反，细胞培养物的生长被PSGAG抑制，表明这些化合物可能无法刺激软骨细胞复制，这是组织再生的先决条件。尽管如此，这些观察结果为低分子量PSGAG在治疗马退行性关节疾病中的真正软骨保护作用提供了直接证据。
Low molecular weight polysulfated glycosaminoglycan (PSGAG) stimulated net collagen and glycosaminoglycan synthesis by normal and arthritic equine fetlock cartilage tissues in organ culture. Arthritic tissues were more sensitive to PSGAG stimulation. The rates of cartilage-specific type-II collagen and chondroitin sulfate-rich glycosaminoglycan synthesis by confluent chondrocyte cell cultures obtained from normal and arthritic equine cartilage tissues were increased by 25 and 50 mg of PSGAG/ml. Cells from arthritic cartilage were also more sensitive to the presence of PSGAG. In addition, concentrations of PSGAG (25 and 50 mg/ml) approximate to those in synovial fluid after intra-articular injection of 250 mg of PSGAG inhibited the rate of collagen and glycosaminoglycan degradation in cell culture. These findings suggest that PSGAG may have a role in the healing of mild cartilage degeneration by encouraging the production of replacement hyaline matrix materials, while delaying their subsequent degradation. In contrast, growth of cell cultures was inhibited by PSGAG, suggesting that these compounds may fail to stimulate chondrocyte replication, a prerequisite for tissue regeneration. Nonetheless, these observations provide direct evidence of a truly chondroprotective role for low molecular weight PSGAG in the treatment of equine degenerative joint disease.