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硫酸化壳寡糖 II(SCOS II)通过 NF-κB 通路抑制 TNF 诱导的软骨肉瘤细胞胶原降解。

Sulfated chitooligosaccharide II (SCOS II) suppress collagen degradation in TNF-induced chondrosarcoma cells via NF-κB pathway.

机构信息

Marine Bioprocess Research Center, Pukyong National University, Busan, Republic of Korea.

出版信息

Carbohydr Res. 2012 Mar 1;350:55-61. doi: 10.1016/j.carres.2011.12.028. Epub 2012 Jan 8.

DOI:10.1016/j.carres.2011.12.028
PMID:22264629
Abstract

Chitooligosaccharides (COS), the hydrolyzed product of chitosan and its derivatives, are known to have interesting pharmaceutical and medicinal applications due to its high solubility, non-toxicity, and increased functionality. Among them sulfated chitooligosaccharides (SCOSs) have been identified to possess enhanced biological activities. This study reports the effects of SCOSs with different molecular weights on the degradation of articular cartilage through unregulated collagenase expression. The results indicated that the SCOS II (3-5kDa) effectively inhibited the expressions of collagenases 1 and 3 and thereby prevented TNF-α induced degradation of collagen in human chondrosarcoma cells (SW-1353). Moreover, the signaling cascade responsible for this effect was found as SCOS II mediated suppression of NF-κB activation. Based on these data, it can be concluded that SCOS II prevented collagen degradation by inhibiting collagenases 1 and 3 via suppressing TNF-α induced NF-κB signaling. We suggest that SCOS II can be further studied as a potential candidate for the treatment of arthritis.

摘要

壳寡糖(COS)是壳聚糖及其衍生物的水解产物,由于其高溶解性、低毒性和增强的功能而具有有趣的药物和医学应用。其中,硫酸化壳寡糖(SCOS)已被确定具有增强的生物活性。本研究报告了不同分子量的 SCOS 通过非调控胶原酶表达对关节软骨降解的影响。结果表明,SCOS II(3-5kDa)有效抑制了胶原酶 1 和 3 的表达,从而防止了 TNF-α诱导的人软骨肉瘤细胞(SW-1353)中胶原的降解。此外,发现了负责这种作用的信号级联反应,即 SCOS II 通过抑制 TNF-α诱导的 NF-κB 信号来抑制 NF-κB 的激活。基于这些数据,可以得出结论,SCOS II 通过抑制 TNF-α诱导的 NF-κB 信号来抑制胶原酶 1 和 3,从而防止胶原降解。我们建议可以进一步研究 SCOS II 作为关节炎治疗的潜在候选药物。

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