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Chondroitin Sulfate
The pathobiology of osteoarthritis and the rationale for using the chondroitin sulfate for its treatment.
Department of Biologia Animale, Biological Chemistry Section, University of Modena and Reggio Emilia, Italy. volpi@unimo.itV olpi N.
Structure-modifying osteoarthritis (OA) drugs are agents that reverse, retard, or stabilize the pathology of OA, thereby providing symptomatic relief in the long-term treatment. The objective of this review is to evaluate the literature on chondroitin sulfate (CS) with respect to the pathobiology of OA to ascertain whether this agent should be classified as a symptomatic slow-acting drug (SYSADOA), a compound that has a slow onset of action and improve OA symptoms after a couple of weeks. CS exhibits a wide range of biological activities and from a pharmacological point of view it produces a slow but gradual decrease of the clinical symptoms of OA and these benefits last for a long period after the end of treatment. Many literature data show that CS could have an anti-inflammatory activity and a chondroprotective action by modifying the structure of cartilage. These properties are also related to the oral adsorption of this molecule as high-molecular mass compounds having clusters of sulfate groups and high charge density capable of exert their chondroprotective activity in vivo.
Chondroitin sulfate extracted from the Styela clava tunic suppresses TNF-alpha-induced expression of inflammatory factors, VCAM-1 and iNOS by blocking Akt/NF-kappaB signal in JB6 cells.
Cancer Lett. 2008 Jun 8;264(1):93-100. Epub 2008 Mar 4.
Xu CX, Jin H, Chung YS, Shin JY, Woo MA, Lee KH, Palmos GN, Choi BD, Cho MH.
Laboratory of Toxicology, College of Veterinary Medicine, Seoul National University, Seoul, Republic of Korea.
Inflammatory mediators are known to play a key role in tumorigenesis, therefore, it is a promising strategy to inhibit the inflammation for cancer prevention and/or treatment. Current study was performed to investigate the effects of chondroitin sulfate (CS) extracted from Styela clava tunic on TNF-alpha-induced inflammation and to elucidate the mechanism of CS on the regulation of inflammatory factors in JB6 cells. Our results showed that CS inhibited TNF-alpha-induced NF-kappaB activation and subsequent vascular cell adhesion molecule 1 and inducible nitric oxide synthase expressions by blocking Akt signals in JB6 cells. Our results suggest that CS may be developed as an effective anti-inflammatory agent in the future.
Proteoglycan development