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

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.
AuthorsBoMi Ryu, S W A Himaya, Romauli J Napitupulu, Tae-Kil Eom, Se-Kwon Kim
JournalCarbohydrate research (Carbohydr Res) Vol. 350 Pg. 55-61 (Mar 01 2012) ISSN: 1873-426X [Electronic] Netherlands
PMID22264629 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCrown Copyright © 2012. Published by Elsevier Ltd. All rights reserved.
Chemical References
  • NF-kappa B
  • Oligosaccharides
  • Sulfates
  • Tumor Necrosis Factor-alpha
  • Collagen
  • Collagenases
Topics
  • Chondrocytes (cytology, drug effects, metabolism)
  • Chondrosarcoma (pathology)
  • Collagen (metabolism)
  • Collagenases (metabolism)
  • Gene Expression Regulation, Enzymologic (drug effects)
  • Humans
  • Molecular Weight
  • NF-kappa B (metabolism)
  • Oligosaccharides (chemistry, pharmacology)
  • Proteolysis (drug effects)
  • Signal Transduction (drug effects)
  • Sulfates (chemistry)
  • Tumor Necrosis Factor-alpha (pharmacology)

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